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PubMed1992

Accelerated decay of the cell bound C4b2a complex by serum of patients with membranoproliferative glomerulonephritis and acute poststreptococcal glomerulonephritis.

Serum from patients with membranoproliferative glomerulonephritis (MPGN) and acute poststreptococcal glomerulonephritis (APSGN) accelerated the decay of the cell bound C4b2a (C42) and C4b hemolytic activity relative to pooled normal human serum (pNHS) after 5 min incubation at 30 degrees C in EDTA-GVB. The accelerated decay of the C42 hemolytic activity was heat stable (56 degrees C 30 min) and was inhibited by monoclonal antibody against human C4 binding protein (MoAb:C4BP) or C4 binding protein (C4BP) depleted serum. C4 nephritic factor (C4NeF) was employed to stabilize the labile classical pathway C3 convertase C42 complex. Serum from patients with MPGN and APSGN reduced the C4NeF stabilizing activity. Sera from 32 of 46 patients with MPGN and all of 7 patients with APSGN reduced the C42 hemolytic activity relative to 50 normal human serum (NHS) after 5 min incubation at 30 degrees C in EDTA-GVB, and there was no relationship with the serum concentration of C4BP. In vivo, accelerated decay of C42 convertase might interfere with the clearing and processing mechanism of circulating immune complexes (IC) by reducing deposition of C3b on the IC lattice.

Acute Disease↗

PubMed1988

Does bacillus Calmette-Guérin immunotherapy accelerate growth and cause metastatic spread of second primary malignancy?

In our study, 29 of 150 patients with bladder cancer also had other associated primary malignancies, 10 of which were manifested after intravesical treatment with bacillus Calmette-Guérin (BCG). Second primary malignancies developed in 5 of these patients within three months of the start of BCG therapy. All 5 showed acceleration of the second primary tumor, and distant metastatic lesions developed in 4. In the other 5 patients nonbladder primary malignancies developed eight months or more after intravesical BCG therapy started, but did not show acceleration or spread. Twenty patients with other primary malignancies that had developed months to years before intravesical therapy did not show acceleration or spread of those tumors. We have seen enough cases of patients who received intravesical BCG at the time of growth and spread of second primary malignancies to warrant concern. Animal and human studies of BCG use for treatment of malignancy indicate that the temporal relationship between the starting point of tumor development and the starting point of BCG treatment is crucial in determining whether BCG will eradicate or exacerbate the tumor. We have therefore instituted a change in our treatment until the question of whether or not BCG causes the appearance and spread of these second malignancies is answered.

Administration, Intravesical↗

PubMed1993

Effect of cocaine on the production of puberty-accelerating pheromone by male mice.

This study examined whether chronic cocaine exposure could reduce reproductive fitness of adult male mice by interfering with their production of the puberty-accelerating pheromone, an androgen-dependent urinary pheromone that accelerates puberty in juvenile female mice. Administered at a high dose of 60 mg/kg body weight/day, cocaine caused mortality, body weight loss, and suppression of circulating testosterone during the first week of treatment. However, at 40 mg/kg/day, it resulted in little adverse effect on these parameters. Animals showed habituation to repeated cocaine exposure by regaining part of the lost weight and reelevating suppressed testosterone level at later stages of treatment. Urine samples collected from animals receiving 60 mg/kg cocaine daly for 2 weeks lost the puberty-accelerating effect. However, neither a 3-day treatment of the same dose nor a lower dose of 40 mg/kg reduced the effectiveness. The diminished effect of cocaine-treated male mouse urine might reflect lowered testosterone levels with a lag of 10 to 15 days, similar to that of castrated male mouse urine. These results indicate that cocaine has no direct effect on the production of priming pheromone, and its metabolites in the urine did not affect the response of juvenile females to the pheromone.

Animals↗

PubMed1995

Effect of YM796, a novel muscarinic agonist, on the impairment of passive avoidance response in senescence-accelerated mice.

We compared the effects of YM796 [(-)-S-2,8-dimethyl-3-methylene-1-oxa-8- azaspiro[4,5]-decane L-tartrate monohydrate], a novel muscarinic agonist, on passive avoidance response with those of the cholinomimetics AF102B [(+/-)-cis-2-methylspiro-(1,3-oxathiolane-5,3')-quinuclidine hydrochloride] and NIK247 [9-amino-2,3,5,6,7,8-hexahydro1H-cyclopenta(b)- quinoline monohydrate hydrochloride] in senescence-accelerated mice. SAMP8@YAN (SAM-P/8, senescence-accelerated-prone substrain) showed an age-dependent shortening in the latency of step-through when compared with SAMR1/YAN (SAM-R/1, senescence-accelerated-resistant substrain). The shortened latency of step-through in SAMP8@YAN was prolonged by administration of YM796 (0.3 and 1 mg/kg, PO), AF102B (3 and 10 mg/kg PO), and NIK247 (30 mg/kg, PO) in a bell-shaped manner. In contrast, amitriptyline (10, 30, and 50 mg/kg, PO), with cholinolytic properties, had no effect on this shortened latency of step-through. These results suggest that YM796, AF102B, and NIK247 ameliorated the disturbance of learning behavior, presumably due to facilitation of the central cholinergic system in SAMP8@YAN mice and that SAMP8@YAN may be an appropriate age-dependent model of amnesia for evaluating pharmacological actions of drugs.

Aging↗

PubMed1994

Nicotine improves cognitive disturbance in senescence-accelerated mice.

Senescence-accelerated mice (SAM), a murine model of age-related deterioration in learning ability, were studied as to the acetylcholine (ACh) contents in the brain tissues and the effect of nicotine administration. We found that the ACh content of SAM-P/8 (accelerated senescence-prone) mice was lower than that of SAM-R/1 (accelerated senescence-resistant) mice in the midbrain thalamus and the hypothalamus. In addition, an IP administration of nicotine was found to improve learning ability of SAM-P/8 as shown by performance of a passive avoidance task. Nicotine may potentiate cognitive function in SAM-P/8.

Acetylcholine↗

PubMed1985

Effects of accelerated growth during rearing on reproduction and lactation in ewes lambing at 13 to 15 months of age.

Three trials were conducted using ewe lambs to determine the effects of accelerated growth during rearing on reproduction and lactation. Data were obtained on 113 ewes. Early weaned ewe lambs were randomly assigned to the following prebreeding treatments: (1) thin (T, moderate gain) and (2) fat (F, accelerated gain). They were bred to lamb at 13 to 15 months of age. After breeding, one half of the ewes on the T and F treatments were switched to the other treatment so that postbreeding treatments were TT, TF, FF and FT. Prebreeding treatment did not affect conception rate (T, 95%; F, 96%), but lambing rates were 43, 28 and 27% higher (P<0.05) for F than T ewes in trials 1, 2 and 3, respectively. Daily milk production was higher in T ewes than F ewes for each trial, but the differences were significant only in trial 3. Estimated daily milk yields over the 60-day period were: T ewes, 1482, 1571, 1614 g; F ewes, 1183, 1373, 1321 g for trials 1, 2 and 3, respectively. Number of alveoli also favored T ewes. Switching ewes to the alternate treatment after breeding did not affect reproduction or milk production. Correlations between weight to height ratio and milk yield were negative in trials 1 and 3 but were positive in trial 2. There was no indication that serum T(4) levels affected milk production or reproduction. The results of this study show that accelerated growth during rearing increased lambing rate but may impair milk production. These effects appeared to be fixed by the time the ewes were bred.

Journal Article↗

PubMed1991

Noninvasive acceleration measurements to characterize the pharyngeal phase of swallowing.

Swallowing disorder (dysphagia) presents a major problem in the rehabilitation of stroke and head injured patients. In the present investigation, a new technique is developed for noninvasive assessment of the pharyngeal phase of the swallowing mechanism. Acceleration was measured with two ultra-miniature accelerometers placed on the skin over the throat. Simultaneously, the swallow suction pressure was monitored. Swallowing in normal individuals gave rise to a characteristic acceleration pattern which was quite reproducible, and was in phase with the swallow pressure. In dysphagic patients, the acceleration response was either absent or significantly delayed. The accelerometry technique provides a tool for continuing patient assessment and demonstrating the clinical improvements.

Biomechanical Phenomena↗

PubMed1981

Acceleration of blood in the aorta: a parameter useful for evaluating cardiotonic and afterload reducing substances.

Peak acceleration of blood in the aorta was measured in chloralose-urethane anesthetized open-chest cats with an electromagnetic flow probe around the aortic root. The effects of substances used in the treatment of chronic congestive heart failure were evaluated in this model. Isoprenaline, noradrenaline, and ouabain increased peak acceleration dose-dependently, while blood pressure, cardiac output, and heart rate were influenced differently by each drug. Nitroglycerin and nitroprusside sodium, afterload reducing agents used for the treatment of congestive heart failure, also increased peak acceleration; an effect that in the case of nitroprusside sodium was shown to be mediated by beta-receptors and probably attributable to baroreceptor activation. This simple model was judged to be suitable for evaluating positive inotropic and afterload reducing substances as long as its low sensitivity to heart rate increasing interventions is correctly appreciated.

Animals↗

PubMed1986

Mercury, silver, and gold inhibition of selenium-accelerated cysteine oxidation.

In vivo, cysteine in proteins or glutathione is the major amino acid involved in sulfhydryl oxidation-reduction reactions. An in vitro model of cysteine oxidation accelerated by selenium compounds was used to study the interaction of selenocystine and sodium selenite with metal ions. The interaction of metal ions with selenium compounds inhibited cysteine oxidation. The ionic forms of three toxic soft-acid metals, mercury, silver, and gold, were the most effective inhibitors. The antiarthritic gold drugs, aurothiomalate and aurothioglucose, were of particular interest as they inhibit the activity of selenium-glutathione peroxidase. The effect of gold ligands on gold(I) inhibition of selenocystine-accelerated cysteine oxidation was tested. Sodium cyanide partially reversed inhibition and potassium iodide had no effect. Inhibition of selenium-accelerated oxidation-reduction reactions by soft-acid metal ions may be of biological relevance during toxicities or during antiarthritic gold therapy.

Cysteine↗

PubMed1991

Early anti-HBs antibody response to accelerated and to conventional hepatitis B vaccination regimens in healthy persons.

A significantly higher prevalence of a protective concentration of anti-HBs was achieved at 1 and 2 months among 132 healthy medical students who received an accelerated vaccination schedule with a recombinant hepatitis B vaccine (Engerix-B) than among 120 medical students who received a conventional regimen. With the accelerated schedule, however, 60% students at 1 month and 27% at 2 months were still unprotected (anti-HBs titre less than 10.0 IU/l). Additional passive immunisation should therefore continue to be offered if the accelerated schedule is adopted for post-exposure prophylaxis.

Adult↗

PubMed1984

Accelerated loss of motor neurons in the brachial lateral motor column in muscular dystrophic chicks.

We have examined the development of the brachial lateral motor column in White Leghorn chickens that are homozygous for muscular dystrophy. We found an accelerated loss of motor neurons between days 6 and 11 in ovo in the dystrophic embryos such that at the end of this time they had only 80% of the population in age-matched controls. After day 11 in ovo the rate of motor neuron loss was the same in both normal and dystrophic birds. To determine whether the accelerated motor neuron loss was due to expression of the dystrophic gene within the spinal cord itself or whether it was secondary to abnormalities in some other tissue, we exchanged the brachial region of the spinal cord between normal and dystrophic embryos at 2 days in ovo, allowed the resulting chimeras to develop until 11 days in ovo and estimated the motor neuron population in the transplanted segment of cord. We found that spinal cords transplanted into normal hosts had significantly higher populations of motor neurons than spinal cords transplanted into dystrophic hosts. We concluded that the accelerated motor neuron loss seen in dystrophic birds is not intrinsic to the cord but is influenced by other tissues in the embryo.

Animals↗

PubMed1984

Alkylboronic acids accelerate affinity labelling of acetylcholinesterase with N,N-dimethyl-2-phenylaziridinium ion.

The kinetics of acetylcholinesterase alkylation with N,N-dimethyl-2-phenylaziridinium ion, the anionic-site-directed affinity label, has been investigated in the presence of alkylboronic acids, which are known as the esteratic-site-directed reversible inhibitors of the enzyme. The ternary complex of the enzyme, the aziridinium ion and alkylboronic acid, are formed in this reaction. In the case of propylboronic acid, for which the complete kinetic analysis of the acceleration effect has been carried out, the 85-fold increase in the rate of the enzyme alkylation reaction has been found. This acceleration effect was connected with the alkylation step, whereas the non-covalent binding of the aziridinium ion in the enzyme active centre was even hindered by the alkylboronic acid. The possible mechanism of this kinetic acceleration phenomenon is discussed with special reference to the kinetic data for the spontaneous solvolysis reaction of the aziridinium ion in water and organic solvents.

Acetylcholinesterase↗

PubMed1989

Accelerated idioventricular rhythm complicating atrioventricular junction ablation for automatic atrial tachycardia.

A 13-year-old male with histologic evidence of cardiomyopathy, drug-refractory primary atrial tachycardias, and deteriorating left ventricular function underwent transcatheter His bundle ablation to control ventricular rate. Following an initial successful ablation at the level of the atrioventricular node, the patient exhibited an accelerated escape rhythm of apparent junctional origin (ventricular cycle length = 470 msec, HV = 100 msec) with complete heart block. A second ablation procedure was undertaken, following which an accelerated idioventricular rhythm (cycle length = 500 msec) became apparent and has persisted (follow-up 15 months). Thus, findings in this patient suggest that attempts to control refractory rapid ventricular responses in cardiomyopathy patients with primary atrial tachycardias may be complicated by the potential for junctional and idioventricular sites to exhibit similar abnormally accelerated subsidiary pacemaker function.

Adolescent↗

PubMed1994

Accelerated stability testing of bioproducts: attractions and pitfalls.

Accelerated testing is widely used for the prediction of storage stability and quality, and for the estimation of shelf-lives and 'safe' storage temperatures of labile products. In the food, pharmaceutical and bioindustries, products are stressed by testing at high temperatures. The results are then extrapolated to 'normal' storage conditions. Many such products exist as amorphous solids and are therefore thermodynamically unstable. During accelerated testing, dramatic and sudden physical and/or chemical changes can occur within such products, rendering extrapolation misleading. A knowledge of possible physical changes during heating enables accelerated testing to be performed with confidence.

Biological Products↗

PubMed1990

The selection of patients for accelerated radiotherapy on the basis of tumor growth kinetics and intrinsic radiosensitivity.

Mathematical modeling was used to reach qualitative conclusions concerning the relative rate of local tumor control that might be achieved by using accelerated fractionation to treat only the patients with the most rapidly growing tumors, compared with the control rates that could be expected from either conventional or accelerated radiotherapy alone. The results suggest that concomitant boost therapy is equally or more effective than conventional dose fractionation for all tumors, regardless of their growth kinetics. For tumors with very short clonogen doubling times, CHART (continuous hyperfractionated accelerated radiotherapy) may be even more effective than concomitant boost treatment, but CHART is less effective than conventional or concomitant boost therapy for tumors with longer clonogen doubling times. Thus, there is a rationale for using a predictive assay of tumor clonogen doubling times to identify the patients who should be treated with CHART. However, improvements in local tumor control resulting from concomitant boost treatment or the selective use of CHART are not likely to be apparent in the population as a whole, because the overall control rates are largely determined by refractory tumors having little chance of control with any of the treatments and by highly responsive tumors that are likely to be controlled regardless of the treatment choice. Differences in control rates with different treatment strategies are most apparent in the stochastic fraction of the population, which excludes those patients for whom there is either very little chance (e.g. less than 1%) or a very high chance (e.g. greater than 99%) of achieving local control with both treatments. The stochastic fraction can be approximated by excluding those patients with the most radioresistant and the most radiosensitive tumors, since intrinsic tumor radiosensitivity appears to be the single most important factor determining treatment outcome.

Dose-Response Relationship, Radiation↗

PubMed1991

Physical characterization of acrylic bone cement cured with new accelerator systems.

In the attempt to substitute dimethyl-p-toluidine (DMPT), a toxic tertiary aryl-amine accelerator, into the formulation of acrylic cements, less toxic accelerator systems are developed. These systems consist of benzoyl peroxide (BPO) and unsaturated tertiary-aryl-amines, such as acryloyl- (ANP) and methacryloyl-(MNP) N-phenylpiperazine, which can be chemically incorporated in the polymerizing resin or, at least, result in less leaching from cured materials. In this work compressive mechanical properties and ageing tests for colour stability of acrylic cement cured with BPO and ANP or MNP have been considered. For compressive tests, cylindrical specimens were cured with BPO and equivalent molecular amounts of DMPT, ANP and MNP. Compressive yield stress (sigma y), strain at yield (epsilon y, %) and elastic modulus (E) gave very similar results for samples cured with DMPT and ANP, and slightly lower results for samples cured with MNP. In colour stability tests, the samples (disks of 1.5 cm diameter) were exposed to UV light at different irradiation times (up to 42 h). The evaluation of the colour change was performed with a digital analyser for images, and observed under scanning electron microscopy. From the obtained results, ANP appeared to be the best candidate as accelerator in the preparation of biomedical acrylic resins and composites.

Acrylic Resins↗

PubMed1991

Acceleration of catalase and peroxidase activities in Lemna minor L. and Allium cepa L. in response to low levels of aquatic mercury.

The purpose of this study was to assess certain physiological responses of Lemna minor L. (duckweed) and Allium cepa L. (onion) to aquatic mercury at low concentrations. Following a 96-h exposure of plants to nutrient medium contaminated with known levels of mercuric chloride (HgCl(2)), 0.001 to 4 mg litre(-1) (0.0007 to 2.95 mg Hg litre(-1)) or methyl mercuric chloride (MeHgCl(2)), 0.0001 to 0.1 mg litre(-1) (0.0007 to 0.07 mg Hg litre(-1)), the physiological endpoints measured were the growth of fronds (Lemna minor) or roots (Allium cepa), and catalase and peroxidase activities in both plant assays. The EC(50) for HgCl(2) on the basis of the growth curve of Lemna minor was found to be 2.1 mg litre(-1). HgCl(2) and MeHgCl(2) were lethal to L. minor at concentrations of 4 and 0.01 mg litre(-1), respectively. The range of low concentrations that accelerated growth as well as enzymic activities in L. minor was 0.004 to 0.04 mg litre(-1) for HgCl(2) and 0.001 mg litre(-1) for MeHgCl(2). HgCl(2) and MeHgCl(2) induced maximum enzymic activity in Lemna fronds at concentrations of 0.008 and 0.0005 mg litre(-1), respectively. In Allium roots, catalase activity was accelerated at all the concentrations of HgCl(2) (0.001-2 mg litre(-1)) and MeHgCl(2) (0.0001-0.1 mg litre(-1)) tested. The activity of peroxidase was, however, accelerated by HgCl(2) at concentration range 0.01-1.0 mg litre(-1), or by MeHgCl(2) at 0.001 mg litre(-1). The concentrations of HgCl(2) and MeHgCl(2) that induced the highest enzymic activity in Allium roots were 0.05 mg litre(-1) and 0.001 mg litre(-1), respectively.

Journal Article↗

PubMed1996

Effects of ethylenediurea (EDU) on ozone-induced acceleration of foliar senescence in potato (Solanum tuberosum L.).

Experiments were conducted to examine the effects of the anti-ozonant ethylenediurea (EDU) and chronic ozone (O3) exposure on leaf physiology and senescence in an O3-sensitive potato cultivar (Solanum tuberosum L. cv. Norland). A dose-response experiment showed that an EDU concentration of 15 mg l(-1) soil (given as a soil drench) provided complete protection from accelerated foliar senescence induced by exposure to 0.1 microl l(-1) O3 for 5 h day(-1) for 11 days. EDU doses of 45 and 75 mg active ingredient l(-1) soil also gave protection but were associated with symptoms of toxicity and delayed senescence. In further experiments, plants were given 0 or 15 mg EDU l(-1) soil and exposed to clean air or 0.1 microl l(-1) O3 for 5 h day(-1) for 14 days. Chronic O3 exposure in the absence of EDU resulted in accelerated foliar senescence, characterized by early declines in net photosynthesis and Rubisco quantity in O3-treated plants relative to controls. EDU in the presence of O3 gave complete protection against symptoms of accelerated senescence. Senescence was not delayed in plants that received EDU in the absence of O3, and no symptoms of EDU toxicity were evident. The results suggest that EDU-induced tolerance to O3 was not based on 'anti-senescent' properties of this anti-ozonant.

Journal Article↗