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PubMed1999

Effects of an acidic fibroblast growth factor fragment analog on learning and memory and on medial septum cholinergic neurons in senescence-accelerated mice.

We examined the effects of repeated subcutaneous injections of an acidic fibroblast growth factor fragment analog, [Ala16] acidic fibroblast growth factor (1-29), on learning and memory and on the choline acetyltransferase immunoreactivity of forebrain neurons in senescence-accelerated mice. One group of accelerated senescence-prone mice (accelerated senescence-prone-8) received [Ala16] acidic fibroblast growth factor (1-29), whereas the other group of accelerated senescence-prone-8 mice and a group of accelerated senescence-resistant mice (control) received vehicle solution. Injections began at three weeks after birth and were given weekly for 10 months. In a passive avoidance test, the mean retention latency at three, six and nine months of age was significantly longer in controls (vehicle-treated accelerated senescence-resistant-1) and acidic fibroblast growth factor fragment-treated accelerated senescence-prone-8 than in vehicle-treated accelerated senescence-prone-8 mice, and the latency in acidic fibroblast growth factor fragment-treated accelerated senescence-prone-8 mice was significantly shorter than that in controls only at nine months of age. In the Morris water maze task, the mean latency to climb onto the platform was significantly longer in acidic fibroblast growth factor fragment- and vehicle-treated accelerated senescence-prone-8 mice than in controls. However, the mean latency in the third and fourth trial blocks was significantly shorter for acidic fibroblast growth factor fragment-treated accelerated senescence-prone-8 than for vehicle-treated accelerated senescence-prone-8 mice. In the probe trials, controls and acidic fibroblast growth factor fragment-treated accelerated senescence-prone-8 mice spent significantly more time in the quadrant in which the platform had previously been located than in the other three quadrants. In acidic fibroblast growth factor fragment-treated accelerated senescence-prone-8 mice, the density of medial septum neurons intensely stained for choline acetyltransferase was significantly greater than that in vehicle-treated accelerated senescence-prone-8 mice, but significantly less than that in controls. The results indicate that the beneficial effect of [Ala16] acidic fibroblast growth factor (1-29) on learning and memory function in accelerated senescence-prone-8 mice may be related to a preservation of function in medial septum cholinergic neurons.

Aging↗

PubMed1975

Incidence and description of accelerated ventricular rhythm complicating acute myocardial infarction.

One hundred and nineteen episodes of accelerated ventricular rhythm (less than 125/min) were noted in 37 patinets with acute myocardial infarction during a 1 year period. The incidence was 12.7 per cent. Twenty-seven episodes of fast ventricular tachycardia (less than 125/min) were noted in 16 of these patients. Eighteen patients had anterior myocardial infarction and 19 inferior myocardial infarction. The mechanism of onset of accelerated ventricular rhythm was classified as escape in 65 episodes. Ventricular premature beats were noted close to episodes of accelerated ventricular rhythm in 31 patients and fast ventricular tachycardia in 14 patients. The morphology of accelerated ventricular rhythm was similar to the ventricular premature beats in 27 patients and similar to the fast ventricular tachycardia in 12. In 11 patinets the morphology of ventricular premature beats, accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm is a relatively common complication of both anterior and inferior myocardial infarction. The high incidence of concomitant fast ventricular tachycardia, the frequency of ventricular premature beats with similar morphology and coupling time, and the instances of two arrhythmias having common rate multiples, suggest that at least in some instances accelerated ventricular rhythm may represent an ectopic focus with exit block.

Adult↗

PubMed1993

Noninvasive estimation of regurgitant flow rate and volume in patients with mitral regurgitation by Doppler color mapping of accelerating flow field.

OBJECTIVES: This study was designed to examine the accuracy of proximal accelerating flow calculations in estimating regurgitant flow rate or volume in patients with different types of mitral valve disease. BACKGROUND: Flow acceleration proximal to a regurgitant orifice, observed with Doppler color flow mapping, is constituted by isovelocity surfaces centered at the orifice. By conservation of mass, the flow rate through each isovelocity surface equals the flow rate through the regurgitant orifice. METHODS: Forty-six adults with mitral regurgitation of angiographic grades I to IV were studied. The proximal accelerating flow rate (Q) was calculated by: Q = 2 pi r2.Vn, where pi r2 is the area of the hemisphere and Vn is the Nyquist velocity. Radius of the hemisphere (r) was measured from two-dimensional or M-mode Doppler color recording. From the M-mode color study, integration of accelerating flow rate throughout systole yielded stroke accelerating flow volume and mean flow rate. Mitral regurgitant flow rate and stroke regurgitant volume were measured by using a combination of pulsed wave Doppler and two-dimensional echocardiographic measurements of aortic forward flow and mitral inflow. RESULTS: The proximal accelerating flow region was observed in 42 of 46 patients. Maximal accelerating flow measured from either two-dimensional (372 +/- 389 ml/s) or M-mode (406 +/- 421 ml/s) Doppler color study tended to overestimate the mean regurgitant flow rate (306 +/- 253 ml/s, p < 0.05). Mean Doppler accelerating flow rate correlated well with mean regurgitant flow rate (r = 0.95, p < 0.001), although there was a tendency toward slight overestimation of mean regurgitant flow by mean accelerating flow in severe mitral regurgitation. However, there was no significant difference between the mean accelerating flow rate (318 +/- 304 ml/s) and the mean regurgitant flow rate (306 +/- 253 ml/s, p = NS) for all patients. A similar relation was found between accelerating flow stroke volume (78.27 +/- 62.72 ml) and regurgitant flow stroke volume (76.06 +/- 59.76 ml) (r = 0.95, p < 0.001). The etiology of mitral regurgitation did not appear to affect the relation between accelerating flow and regurgitant flow. CONCLUSIONS: Proximal accelerating flow rate calculated by the hemispheric model of the isovelocity surface was applicable and accurate in most patients with mitral regurgitation of a variety of causes. There was slight overestimation of regurgitant flow rate by accelerating flow rate when the regurgitant lesion was more severe.

Blood Flow Velocity↗

PubMed2001

Acceleration of the calcaneus at heel strike in neutrally aligned and pes planus feet.

OBJECTIVE: The purpose of this research was twofold: (1) to study the impulsive acceleration of the calcaneus at heel strike in subjects with neutrally aligned (i.e., normal) feet and (2) to explore how the acceleration may differ in subjects with pes planus (i.e., flat) feet. The component of the acceleration vector aligned with the long axis of the tibia was quantified. DESIGN: Subjects with either foot type were instrumented and calcaneal acceleration was quantified during comfortable cadence locomotion. BACKGROUND: Aberrant peak acceleration has been associated with osteoarthritis. While tibial acceleration has been quantified, calcaneal acceleration has not. Additionally, foot morphology, or foot type, has demonstrated an effect on foot function and thus there may be differences in calcaneal acceleration between foot types. METHODS: Six subjects with neutrally aligned feet and six with pes planus feet were selected via a clinical exam. Accelerometers were attached to the posterior aspect of the medial surface of the calcanei bilaterally and 10 walking trials were collected.Results. The average baseline-to-peak acceleration for the neutrally aligned and pes planus feet was 4.79 g (SD, 2.14 g) and 5.24 g (SD, 3.28 g), respectively; the peak-to-peak acceleration was 5.03 g (SD, 2.74 g) and 6.75 g (SD, 3.89 g). There were no significant differences (P>0.05) between foot types. CONCLUSIONS: The calcaneal acceleration at heel strike for neutrally aligned and pes planus feet was not sensitive to foot type. RELEVANCE: Aberrant acceleration has been associated with the development of osteoarthritis [J. Biomech. 5 (3) (1972) 267; J. Biomech. 6 (1) (1973) 51; J. Biomech. 15 (7) (1982) 487]. Osteoarthritis at the subtalar joint, as well as the ankle and midtarsal joints, may be initiated and/or perpetuated by excessive calcaneal acceleration at heel strike.

Acceleration↗

PubMed2002

Accelerated hyperfractionation (AHF) compared to conventional fractionation (CF) in the postoperative radiotherapy of locally advanced head and neck cancer: influence of proliferation.

Based on the assumption that an accelerated proliferation process prevails in tumour cell residues after surgery, the possibility that treatment acceleration would offer a therapeutic advantage in postoperative radiotherapy of locally advanced head and neck cancer was investigated. The value of T(pot) in predicting the treatment outcome and in selecting patients for accelerated fractionation was tested. Seventy patients with (T2/N1-N2) or (T3-4/any N) squamous cell carcinoma of the oral cavity, larynx and hypopharynx who underwent radical surgery, were randomized to either (a) accelerated hyperfractionation: 46.2 Gy per 12 days, 1.4 Gy per fraction, three fractions per day with 6 h interfraction interval, treating 6 days per week or (b) Conventional fractionation: 60 Gy per 6 weeks, 2 Gy per fraction, treating 5 days per week. The 3-year locoregional control rate was significantly better in the accelerated hyperfractionation (88 +/- 4%) than in the CF (57+/- 9%) group, P=0.01 (and this was confirmed by multivariate analysis), but the difference in survival (60 +/- 10% vs 46 +/- 9%) was not significant (P=0.29). The favourable influence of a short treatment time was further substantiated by demonstrating the importance of the gap between surgery and radiotherapy and the overall treatment time between surgery and end of radiotherapy. Early mucositis progressed more rapidly and was more severe in the accelerated hyperfractionation group; reflecting a faster rate of dose accumulation. Xerostomia was experienced by all patients with a tendency to be more severe after accelerated hyperfractionation. Fibrosis and oedema also tended to be more frequent after accelerated hyperfractionation and probably represent consequential reactions. T(pot) showed a correlation with disease-free survival in a univariate analysis but did not prove to be an independent factor. Moreover, the use of the minimum and corrected P-values did not identify a significant cut-off. Compared to conventional fractionation, accelerated hyperfractionation did not seem to offer a survival advantage in fast tumours though a better local control rate was noted. This limits the use of T(pot) as a guide for selecting patients for accelerated hyperfractionation. For slowly growing tumours, tumour control and survival probabilities were not significantly different in the conventional fractionation and accelerated hyperfractionation groups. A rapid tumour growth was associated with a higher risk of distant metastases (P=0.01). In conclusion, tumour cell repopulation seems to be an important determinant of postoperative radiotherapy of locally advanced head and neck cancer despite lack of a definite association between T(pot) and treatment outcome. In fast growing tumours accelerated hyperfractionation provided an improved local control but without a survival advantage. To gain a full benefit from treatment acceleration, the surgery-radiotherapy gap and the overall treatment time should not exceed 6 and 10 weeks respectively.

Adult↗

PubMed2003

Attenuation of human neck muscle activity following repeated imposed trunk-forward linear acceleration.

It has been suggested that, after a passive linear acceleration of a seated subject which resembles a small, rear-end car impact, sensory information from proprioceptive, vestibular, and visual systems elicit stabilizing neck muscular responses. These neck muscular responses are presumably reflex based and are modified with the magnitude of the perturbation. A key issue that remains is to determine whether the neck and head postural responses can be modulated by a previous experience of the acceleration and not only by the magnitude of the acceleration. This question is of interest because, contrary to cadaver studies, one could expect that humans apprehending a rapid trunk acceleration would adopt a bracing behavior to minimize head movements. The aim of the present experiment was to verify whether neck-muscle activities can be modulated when prior knowledge about whole-body acceleration onset, direction, and magnitude are unknown compared with when only acceleration onset is unknown. Nine seated subjects were submitted to 11 imposed, forward linear accelerations (1.1 g). For the first trial, subjects were completely unaware of the platform acceleration characteristics (onset, direction, amplitude, and acceleration magnitude). For the subsequent ten trials, subjects knew they would be submitted to a forward linear acceleration, but the onset of the acceleration was unknown. Head kinematics and EMG responses of the neck muscles to the first perturbation were similar for all subjects (6.2 degrees head extension, EMG activity starting from 55 to 72 ms after platform onset). Following the first trial, however, all subjects showed a decreased neck EMG activity. Moreover, subjects responded in one of two ways across trials: one group of subjects ( n=5) maintained a constant head angular position and velocity, whereas the other group ( n=4) showed an increased head angular position (up to 12.6 degrees ) and velocity. This suggests that the first perturbation trial revealed a completely reactive response. After this initial trial, the responses observed may present a mixture of feedforward and feedback control. It is likely that whiplash injuries occur under conditions resembling those observed for the first trial only. If this is the case, the behavior for the following trials cannot be representative of injury mechanisms occurring in whiplash-like motion. Altogether, our results strongly suggest that, following repeated trunk linear accelerations of a constant magnitude, the nervous system prefers to minimize muscle stress instead of adopting a bracing strategy.

Acceleration↗

PubMed2006

Basic concepts in plasma accelerators.

In this article, we present the underlying physics and the present status of high gradient and high-energy plasma accelerators. With the development of compact short pulse high-brightness lasers and electron and positron beams, new areas of studies for laser/particle beam-matter interactions is opening up. A number of methods are being pursued vigorously to achieve ultra-high-acceleration gradients. These include the plasma beat wave accelerator (PBWA) mechanism which uses conventional long pulse ( approximately 100 ps) modest intensity lasers (I approximately 10(14)-10(16) W cm(-2)), the laser wakefield accelerator (LWFA) which uses the new breed of compact high-brightness lasers (<1 ps) and intensities >10(18) W cm(-2), self-modulated laser wakefield accelerator (SMLWFA) concept which combines elements of stimulated Raman forward scattering (SRFS) and electron acceleration by nonlinear plasma waves excited by relativistic electron and positron bunches the plasma wakefield accelerator. In the ultra-high intensity regime, laser/particle beam-plasma interactions are highly nonlinear and relativistic, leading to new phenomenon such as the plasma wakefield excitation for particle acceleration, relativistic self-focusing and guiding of laser beams, high-harmonic generation, acceleration of electrons, positrons, protons and photons. Fields greater than 1 GV cm(-1) have been generated with monoenergetic particle beams accelerated to about 100 MeV in millimetre distances recorded. Plasma wakefields driven by both electron and positron beams at the Stanford linear accelerator centre (SLAC) facility have accelerated the tail of the beams.

Computer Simulation↗

PubMed2002

Mechanical power output during running accelerations in wild turkeys.

We tested the hypothesis that the hindlimb muscles of wild turkeys (Meleagris gallopavo) can produce maximal power during running accelerations. The mechanical power developed during single running steps was calculated from force-plate and high-speed video measurements as turkeys accelerated over a trackway. Steady-speed running steps and accelerations were compared to determine how turkeys alter their running mechanics from a low-power to a high-power gait. During maximal accelerations, turkeys eliminated two features of running mechanics that are characteristic of steady-speed running: (i) they produced purely propulsive horizontal ground reaction forces, with no braking forces, and (ii) they produced purely positive work during stance, with no decrease in the mechanical energy of the body during the step. The braking and propulsive forces ordinarily developed during steady-speed running are important for balance because they align the ground reaction force vector with the center of mass. Increases in acceleration in turkeys correlated with decreases in the angle of limb protraction at toe-down and increases in the angle of limb retraction at toe-off. These kinematic changes allow turkeys to maintain the alignment of the center of mass and ground reaction force vector during accelerations when large propulsive forces result in a forward-directed ground reaction force. During the highest accelerations, turkeys produced exclusively positive mechanical power. The measured power output during acceleration divided by the total hindlimb muscle mass yielded estimates of peak instantaneous power output in excess of 400 W kg(-1) hindlimb muscle mass. This value exceeds estimates of peak instantaneous power output of turkey muscle fibers. The mean power developed during the entire stance phase increased from approximately zero during steady-speed runs to more than 150 W kg(-1) muscle during the highest accelerations. The high power outputs observed during accelerations suggest that elastic energy storage and recovery may redistribute muscle power during acceleration. Elastic mechanisms may expand the functional range of muscle contractile elements in running animals by allowing muscles to vary their mechanical function from force-producing struts during steady-speed running to power-producing motors during acceleration.

Acceleration↗

PubMed1999

Effects of linear acceleration on fish behavior and eye movements.

Behavioral responses and eye movements of fish during linear acceleration were reviewed. It is known that displacement of otoliths in the inner ear leads to body movements and/or eye movements. On the ground, the utriculus of the vestibular system is stimulated by otolith displacement caused by gravitational and inertial forces during horizontal acceleration of whole body. When the acceleration is imposed on the fish's longitudinal axis, the fish showed nose-down and nose-up posture for tailward and noseward displacement of otolith respectively. These responses were understood that the fish aligned his longitudinal body axis in a plane perpendicular to the direction of resultant force vector acting on the otoliths. When the acceleration was sideward, the fish rolled around his longitudinal body axis so that his back was tilted against the direction in which the inertial force acted on the otoliths. Linear acceleration applied to fish's longitudinal body axis evoked torsional eye movement. Direction of torsion coincided with the direction of acceleration, which compensate the change of resultant force vector produced by linear acceleration and gravity. Torsional movement of left and right eye coordinated with each other. In normal fish, both sinusoidal and rectangular acceleration of 0.1G could evoke clear eye torsion. Though the amplitude of response increased with increasing magnitude of acceleration up to 0.5 G, the torsion angle did not fully compensate the angle calculated from gravity and linear acceleration. Removal of the otolith on one side reduced the response amplitude of both eyes. The torsion angle evoked by rectangular acceleration was smaller than that evoked by sinusoidal acceleration in both normal and unilaterally labyrinthectomized fish. These results suggest that eye torsion of fish include both static and dynamic components.

Acceleration↗

PubMed1982

Intrapartum fetal heart rate monitoring. VI. Prognostic significance of accelerations.

The fetal heart rate (FHR) tracings of 1,996 fetuses were analyzed to assess the prognostic value of accelerations in early labor and just prior to delivery. Accelerations were divided into periodic and sporadic types according to their association or lack of association with uterine contractions. It is shown that two or less sporadic accelerations per 30 minutes are unfavorable. Three accelerations indicate fetal well-being as much as any higher number of accelerations per 30 minutes. FHR abnormalities coexistent with three or more sporadic accelerations were found to have a better prognosis than FHR abnormalities associated with two or less sporadic accelerations. Fetuses exhibiting low FHR variability commonly showed lack of accelerations, whereas normal FHR variability was almost invariably accompanied by sporadic accelerations. The pathogenesis of accelerations is discussed. It is concluded that accelerations are indicators of fetal well-being, whereas the lack of accelerations with lack of reactivity to manipulation of the fetus may be indicative of severe fetal hypoxia with fetal acidemia. This conclusion is supported by fetal outcome and determination of pH from fetal scalp blood.

Apgar Score↗

PubMed1996

Thresholds for detection of motion direction during passive lateral whole-body acceleration in normal subjects and patients with bilateral loss of labyrinthine function.

To investigate the effect of velocity, acceleration, and gradient of acceleration on self-motion perception, thresholds for detection of direction of whole-body interaural acceleration were determined for various stimulus profiles. For acceleration steps, acceleration thresholds at 67% correct detection of motion direction were similar for eight normals (mean 4.84 cm/s2 (range 2.9-6.3), peak gradient = 22 cm/s2) and five labyrinthine-defective subjects (mean 5.65 cm/s2 (4.85-6.6), peak gradient = 25 cm/s2). Velocity thresholds were 7.93 cm/s for a proportion of correct responses of 73% for normals and 9.67 cm/s for 69% of correct detection for avestibular subjects. For linear and parabolic accelerations, high intersubject variability was observed both among nine normals and three labyrinthine-defective subjects. Mean normal and avestibular subjects' acceleration thresholds for 74% of correct responses were respectively 12.1 cm/s2 (7.3-20.4) and 16.4 cm/s2 (13.2-20) for a ramp with gradient of acceleration = 2.8 cm/s3, 19.2 cm/ s2 (10.4-35.3) and 28.2 cm/s2 (21.4-32.8) for a ramp with gradient = 7.9 cm/s3 and 16.7 cm/s2 (10.5-25) and 20.6 cm/s2 (18.4-24.2) for a parabola with second derivative = 1.52 cm/s4. The corresponding velocity thresholds for normals were 21.2 cm/s (5.2-50.3), 22.0 cm/s (7-56.6), and 22.2 cm/s (9.5-43.7). The lowest thresholds were obtained for acceleration steps indicating that a high acceleration gradient facilitates motion perception. For linear and parabolic accelerations, motion perception seemed to follow an integration of acceleration, but a high intersubject variability was observed. For all stimuli, the range of thresholds for normals and avestibular subjects overlapped showing that detection of motion was not a sole prerogative of the otoliths but could also be performed using somatosensory cues.

Adult↗

PubMed1997

Micellar acceleration of oxygen-dependent reactions and its potential use in the study of human low density lipoprotein.

The reaction rate between superoxide and nitro-blue tetrazolium (NBT) is known to be accelerated/catalysed by micellar systems. Previous reports suggest that an accelerated rate of NBT reduction by micellar systems may be the result of either the binding of organic substrates such as NBT to the micellar phase giving a more favourable environment for superoxide reduction (an orientation effect), or the electrostatic interaction between micelles and superoxide. Here we show, using three different superoxide generating systems, that micelles composed of a number of different lipids or human low density lipoprotein (LDL) accelerates the apparent reaction between superoxide and NBT. Evidence in favour of an accelerated production of superoxide as opposed to the accelerated reduction of NBT is provided and we propose that the accelerated production of superoxide is a consequence of increased oxygen solubility in the lipid, rather than aqueous, phase. This is supported by: 1. The absence of any spectrophotometric changes due to interaction between lipid or LDL and reagents used. 2. The ability of micelles composed of a number of different fatty substances, including LDL, to accelerate superoxide generation, assessed by NBT reduction. 3. The behaviour of micelles, which appears to be one of substrate rather than catalyst, during the acceleration of NBT reduction. This is confirmed by the use of a known micellar catalyst, Triton-X100. This suggests that lipids contribute to the reaction as a substrate rather than a catalyst. 4. The inability of LDL to accelerate NBT reduction by potassium superoxide, a reaction which is independent of bimolecular oxygen. 5. The inability of LDL to accelerate NBT reduction when added after superoxide generation. 6. Studies that show LDL can enhance an NBT-independent monitor of oxidation, namely the transition metal-catalysed oxidation of vitamin C. 7. Estimations of the solubility of oxygen in LDL which appear to be consistent with reported physical measurements. Furthermore, we show that LDL modification can alter LDL-mediated micellar acceleration of superoxide generation. Extensive oxidation of LDL decreases micellar acceleration and minimal oxidation enhances it. We suggest that LDL micellar acceleration might serve as a novel approach to studying human LDL.

Humans↗

PubMed1998

Acceleration-induced action potential prolongation and early afterdepolarizations.

INTRODUCTION: Precipitation of torsades de pointes (TdP) has been shown to be associated with acceleration of heart rate in both experimental and clinical studies. To gain insight into the cellular mechanism(s) responsible for the initiation of acceleration-induced TdP, we studied the effect of acceleration of pacing rate in canine left ventricular epicardial, M region, endocardial, and Purkinje fiber preparations pretreated with E-4031, an IKr blocker known to induce the long QT syndrome and TdP. METHODS AND RESULTS: Standard microelectrode techniques were used. E-4031 (1 to 2 microM) induced early after depolarization (EAD) activity in 31 of 36 M cell, 0 of 10 epicardial, 0 of 10 endocardial, and 9 of 12 Purkinje fiber preparations at basic cycle lengths (BCLs) > or = 800 msec. In 30 of 36 M cells, sudden acceleration from a BCL range of 900 to 4,000 msec to a range of 500 to 1,500 msec induced transient EAD activity if none existed before or increased the amplitude of EADs if already present. Acceleration-induced augmentation of EAD activity was far less impressive and less readily demonstrable in Purkinje fibers (4/12). In M cells, appearance of EAD activity during acceleration usually was accompanied by an abbreviation of action potential duration (APD). Within discrete ranges of rates in the physiologic range, acceleration caused a transient prolongation of APD in 38% of M cells, whether or not a distinct EAD was generated. Acceleration produced still more dramatic APD prolongation and EADs in M cells after the BCL was returned to the original slow rate. Epicardium and endocardium APD showed little change immediately after acceleration. A decrease of BCL as small as 10% and, in some cases, a single premature beat could promote EAD activity and APD prolongation in some M cells. Ryanodine (1 microM, 10/10), flunarizine (10 microM, 3/6), and low Na (97 vs 129 mM, 5/5) abolished the acceleration-induced EAD activity and APD prolongation as well as the EAD activity observed at slow rates in M cells pretreated with E-4031. CONCLUSION: Our results suggest that acceleration from an initially slow rate or a single premature beat can induce or facilitate transient EAD activity and APD prolongation in canine ventricular M cell preparations pretreated with an IKr blocker via a mechanism linked to intracellular calcium loading. Our data provide evidence in support of an important contribution of electrogenic Na/Ca exchange current to this process. These acceleration-induced changes can result in the development of triggered activity as well as a marked dispersion of repolarization in ventricular myocardium and, thus, may contribute to the precipitation of TdP in patients with the congenital (HERG defect) and acquired (drug-induced) long QT syndrome.

Action Potentials↗

PubMed2004

A multistage theory of age-specific acceleration in human mortality.

BACKGROUND: Humans die at an increasing rate until late in life, when mortality rates level off. The causes of the late-life mortality plateau have been debated extensively over the past few years. Here, I examine mortality patterns separately for each of the leading causes of death. The different causes of death show distinct mortality patterns, providing some clues about the varying acceleration of mortality at different ages. RESULTS: I examine mortality patterns by first plotting the data of mortality rate versus age on a log-log scale. The slope of the age-specific mortality rate at each age is the age-specific acceleration of mortality. About one-half of total deaths have causes with similar shapes for the age-specific acceleration of mortality: a steady rise in acceleration from midlife until a well-defined peak at 80 years, followed by a nearly linear decline in acceleration. This first group of causes includes heart disease, cerebrovascular disease, and accidental deaths. A second group, accounting for about one-third of all deaths, follows a different pattern of age-specific acceleration. These diseases show an approximately linear rise in acceleration to a peak at 35-45 years of age, followed by a steep and steady decline in acceleration for the remainder of life. This second group includes cancer, chronic respiratory diseases, and liver disease. I develop a multistage model of disease progression to explain the observed patterns of mortality acceleration. CONCLUSIONS: A multistage model of disease progression can explain both the early-life increase and late-life decrease in mortality acceleration. An early-life rise in acceleration may be caused by increasing rates of transition between stages as individuals grow older. The late-life decline in acceleration may be caused by progression through earlier stages, leaving only a few stages remaining for older individuals.

Adult↗

PubMed1998

Off-center yaw rotation: effect of naso-occipital linear acceleration on the nystagmus response of normal human subjects and patients after unilateral vestibular loss.

Dual search coils were used to record horizontal, vertical and torsional eye movement components of one eye during nystagmus caused by off-center yaw rotation (yaw centrifugation). Both normal healthy human subjects (n=7) and patients with only one functioning labyrinth (n=12) were studied in order to clarify how the concomitant linear acceleration affected the nystagmus response. Each subject was seated with head erect on the arm of a fixed-chair human centrifuge, 1 m away from the center of the rotation, and positioned to be facing along a radius; either towards (facing-in) or away from (facing-out) the center of rotation. Both yaw right and yaw left angular accelerations of 10 degrees s(-2) from 0 to 200 degrees/s were studied. During rotation a centripetal linear acceleration (increasing from 0 to 1.24xg units) was directed along the subject's naso-occipital axis resulting in a shift of the resultant angle of the gravitoinertial acceleration (GIA) of 51 degrees in the subject's pitch plane and an increase in the total GIA magnitude from 1.0 to 1.59xg. In normal subjects during the angular acceleration off-center there were, in addition to the horizontal eye velocity components, torsional and vertical eye velocities present. The magnitude of these additional components, although small, was larger than observed during similar experiments with on-center angular acceleration (Haslwanter et al. 1996), and the change in these components is attributed to the additional effect of the linear acceleration stimulation. In the pitch plane the average size of the shift of the axis of eye velocity (AEV) during the acceleration was about 8 degrees for a 51 degrees shift of the GIA (around 16% of the GIA shift) so that the AEV-GIA alignment was inadequate. There was a very marked difference in the size of the AEV shift depending on whether the person was facing-in [AEV shift forward (i.e. non-compensatory) of about 4 degrees] or facing-out [AEV shift forward (i.e. compensatory) of around 12 degrees]. The linear acceleration decreased the time constant of decay of the horizontal component of the post-rotatory nystagmus: from an average of 24.8 degrees/s facing-in to an average of 11.3 degrees/s facing-out. The linear acceleration dumps torsional eye velocity in an manner analogous to, but independent of, the dumping of horizontal eye velocity. Patients with UVD had dramatically reduced torsional eye velocities for both facing-in and facing-out headings, and there was little if any shift of the AEV in UVD patients. The relatively small effects of linear acceleration on human canal-induced nystagmus found here confirms other recent studies in humans (Fetter et al. 1996) in contrast to evidence from monkeys and emphasizes the large and important differences between humans and monkeys in otolith-canal interaction. Our results confirm the vestibular control of the axis of eye velocity of humans is essentially head-referenced whereas in monkeys that control is essentially space-referenced.

Acceleration↗

PubMed1991

Effect of increased acceleration on regional pleural pressure in dogs.

The variation of pleural pressure was measured in anesthetized spontaneously breathing dogs subjected to increased acceleration (0-4 G) in a centrifuge. Two groups of animals were studied. In one group, the resultant acceleration was in a direction either ventral-to-dorsal (+Gx) or dorsal-to-ventral (-Gx), with a relatively small residual cranial-to-caudal acceleration. In the other group, the resultant acceleration was either cranial-to-caudal (+Gz) or caudal-to-cranial (-Gz), with a relatively small residual dorsal-to-ventral acceleration. Pleural liquid pressure (Ppl) was measured by two rib capsules that were separated by 7-9 cm and oriented either in the dorsal-to-ventral or cranial-to-caudal direction. At functional residual capacity, Ppl in the nondependent lung region became more negative when the acceleration was in the +Gx or +Gz direction. Thus the lung would be susceptible to damage that results from overexpansion in these acceleration directions. By contrast, acceleration in the -Gx or -Gz direction produced values of Ppl at functional residual capacity that were positive. Thus, in these acceleration directions, the respiratory muscles must provide greater force during inspiration to overcome lung compression before lung ventilation can occur. The Ppl gradients with respect to the acceleration directions increased approximately in proportion to acceleration in the +Gx, -Gx, and -Gz directions but remained relatively constant in the +Gz direction.

Acceleration↗

PubMed1999

Increased expression of hippocampal cholinergic neurostimulating peptide-related components and their messenger RNAs in the hippocampus of aged senescence-accelerated mice.

Hippocampal cholinergic neurostimulating peptide stimulates cholinergic phenotype development by inducing choline acetyltransferase in the rat medial septal nucleus in vitro. Adult senescence-accelerated-prone mice/8, a substrain of the senescence-accelerated-prone mouse, show a remarkable age-accelerated deterioration in learning and memory. We cloned mouse hippocampal cholinergic neurostimulating peptide precursor protein complementary DNA. The deduced amino acid sequence showed that the neurostimulating peptide itself is the same as that found in the rat. In situ hybridization revealed that the highest expression of the precursor protein messenger RNA was in hippocampal pyramidal neurons. Compared with a strain of senescence-accelerated-resistant mouse (control mouse), adult senescence-accelerated-prone mice/8 showed increased expression of both the precursor messenger RNA and the neurostimulating peptide-related immunodeposits in the hippocampal CA1 field. The deposits were intensely and diffusely precipitated in neuropils throughout the strata oriens and radiatum in senescence-accelerated-prone mice/8, but not in control mice. The neurostimulating peptide content in the hippocampus was higher in senescence-accelerated-prone mice/8 than in control mice, while its precursor protein itself was not different between the two strains. Furthermore, our previous and present data show that the medial septal and hippocampal choline acetyltransferase activity was significantly lower in senescence-accelerated-prone mice/8 than in control mice. The data suggest that, in hippocampal neurons in adult senescence-accelerated-prone mice/8, the production of hippocampal cholinergic neurostimulating peptide precursor protein in neuronal somata, which is associated with an increased expression of its messenger RNA in the CA1 field, occurs as a consequence of low activity in their presynaptic cholinergic neurons. This is followed by accelerated processing to generate bioactive peptide and transport to its functional fields. However, certain mechanisms reduce the release of the peptide and lead to its accumulation in the neuropil. These disturbances of the septohippocampal cholinergic system might be the biochemical mechanism underlying the characteristic deterioration of senescence-accelerated-prone mice/8.

Aging↗

PubMed2000

Evaluation of broiler growth velocity and acceleration in relation to pulmonary hypertension syndrome.

An evaluation was made of the relationship between individual daily growth patterns and susceptibility of broiler chickens to pulmonary hypertension syndrome (PHS). In the first experiment, 46 male broilers were weighed for each of 50 d, during which time 13 developed PHS. Three temporal phases (0 to 15, 16 to 35, and 36 to 50 d) of broiler growth velocity and acceleration were examined. Correlation dimensions and Lyapunov exponents suggested evidence of chaos in growth velocity and acceleration, but the absence of detectable differences between broilers in the normal and PHS categories led us to reject the hypotheses that growth is more chaotic in normal broilers than in broilers susceptible to PHS. Growth velocity and acceleration values for mean and SD were statistically evaluated as response variables for each growth phase. Mean values for velocity during the third phase were different between broilers in the normal and PHS categories (velocity: 68.8 vs 48.9 g/d, P = 0.03, respectively) and (acceleration: 0.3 vs -1.4 g/d2, P = 0.07, respectively). The third phase SD (reflecting oscillation for velocity and acceleration) was greater for normal than for PHS birds (velocity: 26.1 vs 21.3 g/d, P = 0.13, respectively; acceleration: 39.7 vs 28.2 g/d2, P = 0.03, respectively). The hypothesis was accepted that normal birds have greater oscillations in growth velocity and acceleration than birds susceptible to PHS. A general regression neural network (GRNN) with genetic adaptive calibration was trained to predict PHS based on individual growth phases and their combinations. Data representing the first, first two, and all three phases of growth were determined to have potential for computerized diagnostic weighing. With the GRNN, birds in all three data sets were successfully classified (100%) with or without PHS. A third hypothesis, therefore, was accepted that artificial neural networks could be used to distinguish the difference between normal broilers and those susceptible to PHS. In the second experiment, only one bird was diagnosed with PHS. Velocity and acceleration neural networks from Phase 1 and Phases 1 and 2 in the first experiment were applied to the growth velocity and acceleration data of Experiment 2. The Phase 1 neural networks were the most promising in that they correctly identified 71.6 and 72.4% of the birds as normal for velocity and acceleration data, respectively. In general, data in the second experiment exceeded the neural network range of training for both velocity and acceleration, which reflected increased oscillation during the second phase of growth.

Animals↗