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PubMed1984

The relationship between movements and accelerations in fetal heart rate at twenty-four to thirty-two weeks' gestation.

The purpose of this study was to establish the relationship between fetal heart rate accelerations and fetal body movements in fetuses at 24 to 32 weeks' gestation. The results suggest that body movements in younger fetuses do not occur with accelerations that are readily recognizable (i.e., less than 15 bpm), but as fetuses get older, the interaction between body movements and fetal heart rate becomes more evident and accelerations become more recognizable (i.e., greater than or equal to 15 bpm). The data presented suggest that there is a maturational aspect to the relationship between fetal heart rate and fetal body movements as fetuses increase in gestational age from 24 to 32 weeks. The conclusion, therefore, is that the nonstress test, as presently defined for older fetuses, is not valid for gestations below 32 weeks, and new criteria must be established.

Female↗

PubMed1989

The influence of spontaneous accelerations of fetal heart rate on umbilical artery velocity waveforms.

For clinical interpretation of Doppler waveforms, it is important to establish the extent to which fetal heart rate changes affect the umbilical artery velocity waveform. Umbilical artery waveforms were measured with continuous wave ultrasonography during spontaneous accelerations of the fetal heart rate in 20 uncomplicated, near-term pregnancies. On average, an acceleration of 20 beats/min of fetal heart rate within an individual was associated with a reduction in the systolic/diastolic velocity ratio of 0.25. There was, however, considerable variability in the response, and in six patients the systolic/diastolic ratio actually increased with heart rate. We conclude that fetal heart accelerations within the normal range cause only small and variable changes in the systolic/diastolic ratio.

Blood Flow Velocity↗

PubMed1995

Bioprosthetic valve tissue viscoelasticity: implications on accelerated pulse duplicator testing.

Most of our knowledge of heart valve mechanics has been gained from low strain-rate studies much lower than physiologic levels. Using a high-speed materials testing system, we compared the low and high strain-rate viscoelastic behavior of porcine aortic valve cusps at extension rates of up to 40 mm/s. Circumferential and radial strips were stretched and then held in their stretched configuration to measure their "stress-relaxation" behavior. During low strain-rate stretching, only 6% of the initial stress dissipated or relaxed after 1 second, whereas 25% of the stress dissipated during high strain-rate stretching. This considerable difference in stress relaxation suggests a rate-dependent viscoelastic behavior that has not been accounted for in valve design and may have important implications for accelerated pulse testing. Even though the valve cusp is loaded for only 0.4 seconds during each heartbeat, at least 15% of the stress may relax over that period. During accelerated pulse testing, however, sufficient time may not be available to allow the tissue fibers to relax back to their natural state before the subsequent loading cycle, leading to a higher baseline preload. In addition, because valve tissue is not given sufficient time to relax before the next cycle, pulse testing subjects the valves to lower-magnitude cyclic stresses than does physiologic loading. Because both the baseline preload and the magnitude of cyclic stresses may lead to early fatigue failure, accelerated wear testing may either overestimate or underestimate valve durability. Clearly, the mechanism of stress-induced failure of biologic tissues must be elucidated before too much validity is placed on pulse duplicator studies.

Animals↗

PubMed1994

Accelerated net efflux of 3-O-methylglucose from rat adipocytes: a reevaluation.

In a study of 3-O-methylglucose transport in insulin-stimulated rat adipocytes (catalyzed primarily by the GLUT4 isoform), it was reported that at 37 degrees C the Km and Vmax were 2.8-fold higher for net efflux than for equilibrium exchange (Vinten, J. (1984) Biochim. Biophys. Acta 772, 244-250). Because of its implications for the relative sizes of steps in the transport cycle, we reinvestigated this phenomenon. Accelerated net efflux was apparent when the extracellular methylglucose was diluted 26-fold but not when it was diluted 11-fold. When analyzed according to the one-site alternating conformation model, the data indicate about a 1.7-fold higher Vmax for efflux than for exchange, only about 40% of the difference reported previously. Together with other results in the literature, the accelerated net flux indicates that the conformational change of the loaded transporter from its outward-facing to its inward-facing form is likely the slowest step in the transport cycle, in contrast to the case for GLUT1. Experiments at 25 degrees C indicate a lower degree of accelerated net flux than at 37 degrees C. This is consistent with the above conformational change being the step with the lowest activation energy, as for GLUT1.

3-O-Methylglucose↗

PubMed1985

Aluminium salts accelerate peroxidation of membrane lipids stimulated by iron salts.

Aluminium salts do not themselves stimulate peroxidation of ox-brain phospholipid liposomes, but they greatly accelerate the peroxidation induced by iron(II) salts at acidic pH values. This effect of Al(III) is not seen at pH 7.4, perhaps because Al(III) salts form insoluble complexes at this pH in aqueous solution. Peroxidation of liposomes in the presence of Al(III) and Fe(II) salts is inhibited by the chelating agent desferrioxamine, and by EDTA and diethylenetriaminepentaacetic acid at concentrations greater than those of Fe(II) salt. Aluminium salts slightly stimulate the peroxidation of peroxide-depleted linolenic acid micelles, but they do not accelerate the peroxidation induced by addition of iron(II) salts to the micelles at acidic pH. Aluminium salts accelerate the peroxidation observed when human erythrocytes are treated with hydrogen peroxide at pH 7.4. Desferrioxamine decreases the peroxidation. We suggest that Al(III) ions produce an alteration in membrane structure that facilitates lipid peroxidation, and that the increased formation of fluorescent age pigments in the nervous system of patients exposed to toxic amounts of Al(III) may be related to this phenomenon. The ability of desferal to bind both iron (III) and aluminium(III) salts and to inhibit lipid peroxidation makes it an especially useful chelating agent in the treatment of 'aluminium overload'.

Aluminum↗

PubMed1991

Peptides homologous to the amyloid protein of Alzheimer's disease containing a glutamine for glutamic acid substitution have accelerated amyloid fibril formation.

beta-Amyloid (A beta) deposition in fibril form is the central event in a number of diseases, including Alzheimer's disease (AD) and hereditary cerebral hemorrhage with amyloidosis - Dutch type (HCHWA-D). A beta is produced by degradation of a larger amyloid precursor protein (APP). Recently a mutation in the APP gene has been found in HCHWA-D causing a glutamine for glutamic acid substitution at residue 22 of A beta. The influence of this mutation on fibrillogenesis is not known, although it is clear that affected patients have accelerated cerebrovascular amyloid deposition, with disease symptoms early in life. We report the in vitro demonstration of accelerated fibril formation in a 28 residue synthetic peptide homologous to the Dutch variant A beta. Furthermore, in eight residue peptides homologous to A beta the presence of the mutation is necessary for fibril formation. These findings provide a mechanism for accelerated amyloid formation in the Dutch variant of APP.

Alzheimer Disease↗

PubMed1983

Accelerated development of riboflavin deficiency by treatment with chlorpromazine.

The present study was undertaken to determine whether treatment with chlorpromazine accelerates the depletion of tissue stores of flavin adenine dinucleotide during dietary riboflavin deficiency. These investigations derived their impetus from earlier findings that low doses of chlorpromazine in rats fed abundant riboflavin increase urinary riboflavin excretion and reduce hepatic flavin stores. From 6 to 10 days after beginning to feed on a riboflavin-deficient diet, rats treated with chlorpromazine, 2 mg/kg body weight twice daily, had approximately twice the urinary riboflavin excretion of that of pair-fed saline-treated controls. When the riboflavin-deficient diets and chlorpromazine treatments were extended for 3 weeks and the animals killed, FAD levels in liver, kidney, and heart were markedly lower in drug-treated than in saline-treated animals. When studies were extended for 7 weeks, tissue FAD levels in saline-treated animals declined further and were equal to those of chlorpromazine-treated rats after only 3 weeks of dietary deficiency. Thus, chlorpromazine treatment accelerated urinary riboflavin loss and accelerated tissue depletion of FAD levels during dietary riboflavin deficiency. Brain levels of FAD by contrast were relatively resistant to both dietary riboflavin withdrawal and treatment with chlorpromazine. Subsequent studies showed that urinary riboflavin excretion began to increase within 6 hr of treatment with chlorpromazine. It is concluded that significant riboflavin depletion occurs following treatment with low doses of chlorpromazine, both in animals fed a normal diet and in animals fed a riboflavin-deficient diet, particularly during the early stages of deficiency.

Animals↗

PubMed1985

Trifluoperazine and calcium antagonists accelerate cholinergic desensitization in Aplysia neurons.

The onset of desensitization of excitatory acetylcholine responses in isolated, voltage clamped Aplysia RB neurons to microperfused agonist was accelerated by trifluoperazine and the calcium antagonists SKF-525A and D-600. In the absence of these drugs the time course of desensitization is described as the sum of two exponentials plus a constant. All 3 compounds accelerated the fast exponential component of desensitization, but had opposite effects on the slow component: trifluoperazine and SKF-525A accelerated the slow component, whereas this phase was greatly slowed by D-600. These results provide further evidence that the two components of cholinergic desensitization may be independent and influenced by agents which may affect calcium binding to the acetylcholine receptor.

Animals↗

PubMed1986

Angular bundle kindling is accelerated in rats with a genetic predisposition to acoustic stimulus-induced seizures.

Limbic kindling was examined in genetically epilepsy-prone (GEPR) and non-epileptic control rats. The early stage of kindling development was accelerated in both groups of GEPR rats compared to controls. Later stages of kindling were accelerated in GEPR-9 but not GEPR-3 rats. These results indicate that GEPR rats have an enhanced susceptibility to limbic kindling and suggest that limbic brain alterations may contribute to acceleration of the early stage kindling development in GEPR rats.

Acoustic Stimulation↗

PubMed1987

Carbon disulfide axonopathy. Another experimental model characterized by acceleration of neurofilament transport and distinct changes of axonal size.

The role of axonal transport in the development of structural changes of axons can be examined using experimental models. Two different compounds, 2,5-hexanedione (2,5-HD) and carbon disulfide (CS2), cause axonopathies characterized by the formation of neurofilaments (NF) containing enlargements in preterminal regions of central and peripheral axons. These axonopathies are excellent experimental models of the giant axonal neuropathies, a group of acquired and inherited human diseases of the central and peripheral nervous system. We previously reported that following administration of 2,5-HD, transport of NF is accelerated while number of NF and cross-sectional area are decreased in regions of the axon proximal to the enlargements. We proposed that acceleration of NF transport leads to a 'longitudinal' redistribution of NF which are decreased proximally and increased distally where they form the NF containing axonal enlargements. We have now carried out morphometric, transport and immunocytochemical studies in primary visual axons of rats exposed to CS2. NF-containing axonal enlargements were observed in optic tract and superior colliculus and they increased in number in a proximodistal direction. There was no detectable axonal degeneration and the cross-sectional area of axons proximal to the enlargements was decreased. Transport of NF was markedly accelerated. Immunostaining showed that all 3 NF subunits and phosphorylated epitopes of the 200-kDa NF subunit were present in the NF-containing axonal enlargements. All these findings were similar to those previously observed in the 2,5-HD axonopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Axonal transport of neurofilament is accelerated in peripheral nerve during 2,5-hexanedione intoxication.

The neurotoxic compound 2,5-hexanedione (2,5-HD) causes an axonopathy characterized by the presence of neurofilament (NF)-containing enlargements in the preterminal segments of central and peripheral axons. The 2,5-HD axonopathy is a good model for human acquired and inherited giant axonal neuropathies. Recently, we reported that following 2,5-HD administration, axonal transport of NF is markedly and selectively accelerated in the primary visual system. We have now studied slow axonal transport in the sciatic system of rats intoxicated with 0.5% 2,5-HD in drinking water. Following radiolabeling, transported proteins were examined after polyacrylamide gel electrophoresis and fluorography. The bulk of radiolabeled NF subunits was located 30-50 mm from the spinal cord in 2,5-HD treated animals and 10-25 mm in controls. The rate of transport of the three NF subunits was 0.7 mm/day in controls and 1.2 mm/day in 2,5-HD treated animals. The rate of transport of tubulin was not significantly changed. Electrophysiological studies of soleus nerve and muscle showed no evidence of denervation after 6 weeks of intoxication. It is concluded that, following 2,5-HD administration, transport of NF is preferentially accelerated in both central and peripheral axons. A pathogenetic mechanism based on the acceleration of NF transport is proposed, which may explain the formation and the distal or proximal location of NF-containing axonal enlargements in giant axonopathies.

Action Potentials↗

PubMed1990

Giant axonopathy characterized by intermediate location of axonal enlargements and acceleration of neurofilament transport.

It has previously been shown that 2,5-hexanedione (2,5-HD) and its 3,4-dimethyl derivative (3,4-DMHD) induce neurofilamentous accumulations at prenodal sites in distal and proximal, respectively, regions of peripheral axons. For 2,5-HD, neurofilament (NF) transport is accelerated and this is thought to be directly related to the appearance of the axonal enlargements. For 3,4-DMHD, however, the rate of NF transport cannot be assessed owing to the very proximal position of NF accumulation. In the present study, it is shown that administration to rats of 3-methyl-2,5-hexanedione, the structural 'average' of 2,5-HD and 3,4-DMHD, induces NF accumulations at midway axonal positions of the sciatic and optic systems, and results in acceleration of NF in the sections of optic axons proximal to the enlargements. These results suggest that a common mechanism underlies all gamma-diketone neuropathies, and that the proximodistal pattern of axonal enlargements represents pharmacokinetic variables rather than differences in mode of action. The neurotoxicity of gamma-diketones probably arises from pyrrolation of lysine epsilon-amino groups in crucial regions of NF or related proteins responsible for maintaining the proper supramolecular organization of the cytoskeleton. Acceleration of NF transport appears to be a common characteristic of chemically induced axonopathies, regardless of location, and this is contrary to the theory that gamma-diketone-induced NF accumulation results primarily from a progressive cross-linking of NF occurring subsequent to pyrrole formation.

Actins↗

PubMed1994

Characterization of basic fibroblast growth factor-mediated acceleration of axonal branching in cultured rat hippocampal neurons.

We analyzed in more detail the effect of basic fibroblast growth factor (bFGF) on morphogenesis of rat hippocampal neurons in dissociated cell culture. As a result, we found that bFGF selectively promoted the bifurcation and growth of axonal branches without affecting the elongation rate of primary axons. The dendritic outgrowth was rather inhibited by bFGF. These effects of bFGF resulted in increased complexity of axonal trees. The effect of bFGF was concentration dependent (0.1-10 ng/ml) and was abolished by the presence of anti-bFGF neutralizing antibody. The accelerated axonal branch formation in the presence of bFGF was restored to the basal rate following removal of bFGF, suggesting that the action of bFGF is reversible and that the continuous presence is required for bFGF to accelerate the branch formation. bFGF probably works as a progression signal rather than as a triggering signal. The bFGF-mediated acceleration of axonal branch formation was blocked by treatment with heparitinase and by tyrosine inhibitors, herbimycin A and lavendustin A, indicating the importance of heparan sulfate and tyrosine kinase in bFGF signal transduction. Treatment with a protein kinase C activator phorbol-12-myristate-13-acetate did not significantly affect the neurite branching, and the action of bFGF was not blocked by a protein kinase C inhibitor staurosporine. Protein kinase C is unlikely to play a role in branch formation. The novel action of bFGF as a regulator of axonal branching must be a particularly useful model for the study of neuritogenesis and synaptogenesis of brain neurons.

Alkaloids↗

PubMed1996

Acceleration deficit in patients with cerebellar lesions. A study of kinematic and EMG-parameters in fast wrist movements.

Slowness of goal-directed movements is a frequent symptom following cerebellar lesions. So far it has not been demonstrated whether this slowness represents compensation for impaired braking which is a feature of cerebellar dysfunction with the consequence of hypermetria, or whether it is an independent part of cerebellar movement disorder. To resolve this question we tested 18 cerebellar patients in a paradigm where they not only had to perform fast goal-directed wrist flexion movements (amplitudes 5 degrees and 30 degrees) but also wrist flexion movements as fast and large as possible without particular target. In normals antagonist activity is minimal in large movements without target. Although subjects were clinically only mildly affected they regularly showed a 'slowness of movement' resulting from a reduction of peak acceleration. This in turn was due to the reduced generation of agonist activity. Peak velocity was not significantly decreased because the acceleration phase was adequately prolonged. Since these changes were most pronounced in the 'fast' movements without target the compensation hypothesis should be discarded. The reduction of acceleration must at least partially be due to a genuine cerebellar deficiency in the fast generation of agonist activity.

Adolescent↗

PubMed1994

Cimetidine and omeprazole accelerate gastric ulcer healing by an increase in gastrin secretion.

Daily oral administration of cimetidine or omeprazole markedly accelerated the healing of acetic acid-induced gastric ulcers in rats with a limited food intake time. The increased gastric acid secretion induced by daily treatment with histamine affected neither the spontaneous healing of the ulcers nor the healing-promoting actions of both agents. Pretreatment of rats with ulcers with 6-hydroxydopamine significantly inhibited the increase in the antrum gastrin cells, serum gastrin levels and corpus mucosal thickness elicited by repeated administration of cimetidine or omeprazole. Pretreatment with 6-hydroxydopamine did not affect the inhibitory actions of cimetidine and omeprazole on acid secretion, but completely abolished the ulcer healing-promoting actions of both drugs. Daily intraperitoneal administration of pentagastrin accelerated ulcer healing. These results suggest that cimetidine and omeprazole mainly accelerate the healing of gastric ulcers by the trophic action of gastrin via the increase in gastrin secretion, while the inhibition of acid secretion may play a minor role in ulcer healing.

Analysis of Variance↗

PubMed1984

Polyphosphoinositide hydrolysis by phospholipase C is accelerated by thyrotropin releasing hormone (TRH) in clonal rat pituitary cells (GH3 cells).

Thyrotropin releasing hormone (TRH) accelerates the turnover of phosphatidylinositol in GH3 cells ('phospholipid response'). From the analysis of inositol phosphates in the presence of Li+ which inhibits their dephosphorylation, it can be concluded that the hydrolysis of phosphatidylinositol 4,5-biphosphate, and possibly of phosphatidylinositol 4-phosphate by phospholipase C is markedly accelerated by TRH. It appears that this reaction initiates the acceleration of phosphatidylinositol turnover. The specificity of hormonally regulated phospholipase C reaction for polyphosphoinositides has important implications for the potential role of the phospholipid response as a mechanism of membrane signal transduction.

Animals↗

PubMed1987

Intravenous cisapride accelerates delayed gastric emptying and increases antral contraction amplitude in patients with primary anorexia nervosa.

Delayed gastric emptying is common in primary anorexia nervosa. We investigated in 12 patients whether gastric emptying could be accelerated by the prokinetic drug cisapride. Patients were studied on two occasions 1 wk apart and received, under random double-blind conditions, 8 mg of cisapride and placebo intravenously. Gastric emptying of an isotopically labeled semisolid meal and antral motor activity were measured using a dual-headed gamma-camera for 50 min. Emptying was significantly slower (half-emptying time, 50-191 min; median, 121 min) than in 24 healthy volunteers (half-emptying times, 21-119 min; median, 47 min). Cisapride accelerated emptying significantly (p less than 0.001; half-emptying time after cisapride, 22-80 min; median, 42 min). Antral contraction amplitude increased and contraction frequency decreased significantly (p less than 0.001), whereas the propagation velocity of contractions remained unchanged. We concluded that intravenous cisapride accelerates gastric emptying and increases antral contraction amplitude in patients with anorexia nervosa. Whether or not these effects can prove beneficial in diminishing the patients' symptoms and in helping them to gain weight can only be answered from studies involving long-term treatment with cisapride.

Adolescent↗

PubMed1990

Addition of N-acetylcysteine to aqueous model bile systems accelerates dissolution of cholesterol gallstones.

The organic matrix of cholesterol gallstones contains a macromolecular complex of mucin and bilirubin that may inhibit stone dissolution by limiting contact of desaturated bile with crystalline cholesterol. The goal of this study was to determine if the mucolytic agent N-acetylcysteine could accelerate gallstone dissolution in vitro. Paired gallstones were dissolved in either pure taurocholate (140 mM) or ursodeoxycholate (100 mM), or in bovine bile supplemented with either taurocholate or ursodeoxycholate to achieve the same respective bile-salt concentrations. N-acetylcysteine was added to 1 stone from each pair at a concentration of 500 mM in pure bile salts and 100 mM in supplemented bile. Gallstones dissolved significantly faster in bovine bile supplemented with taurocholate or ursodeoxycholate than in pure solutions of the respective bile salts (n = 30, p less than 0.001). N-acetylcysteine significantly accelerated gallstone dissolution in pure solutions of bile acids (n = 30, p less than 0.001 for each) and in supplemented bovine biles (n = 30, p less than 0.001). N-acetylcysteine also significantly increased the frequency of complete gallstone dissolution in taurocholate-supplemented (66.6% vs. 40.0%) and ursodeoxycholate-supplemented (76.6% vs. 50.0%) bile. These results indicate that the mucolytic agent N-acetylcysteine significantly accelerates in vitro gallstone dissolution. We speculate that adjuvant therapy with an appropriate mucolytic agent may potentially increase the efficacy of clinical gallstone dissolution.

Acetylcysteine↗