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PubMed2001

Sexual precocity in boys: accelerated versus slowly progressive puberty gonadotropin-suppressive therapy and final height.

The indication for GnRH analog treatment in boys with central sexual precocity is based mainly on the age of onset of puberty. Our aim was to determine whether the rate of pubertal progression should also be taken into consideration. Included in the study were 81 boys with central sexual precocity: 27 with true precocious puberty (onset at <9 yr) and 54 with early puberty (onset at 9-10.5 yr). At the time of analysis, all had completed puberty, and 66 (22 central precocious puberty, 44 early puberty) had achieved final height. Progression of puberty (Tanner stage 2 to 3) was accelerated (0.5-1.32 yr) in 42 boys (16 central precocious puberty, 26 early puberty) and slow (1.7-2.9 yr) in 39 (11 central precocious puberty, 28 early puberty). The boys with accelerated puberty had significantly elevated T levels (central precocious puberty and early puberty, P < 0.001), faster growth rate (change in height SD score/duration: central precocious puberty, P < 0.05; early puberty, P < 0.01), and faster bone maturation rate (change in bone age/duration: central precocious puberty, P < 0.05; early puberty, P < 0.001). All 42 boys with accelerated puberty were treated with GnRH analog for 2.3-4.2 yr; the duration to completion of puberty and the height gain after therapy was discontinued were similar for the boys with central precocious puberty and early puberty. The 39 boys with slow puberty received no treatment and had a prolonged course of puberty (central precocious puberty, 5.05 +/- 0.3 yr; early puberty, 4.72 +/- 0.77 yr; average normal, 3.5 yr). The final height achieved in the 35 (11 central precocious puberty, 24 early puberty) untreated boys was within the range of their respective target height. The 31 (11 central precocious puberty, 20 early puberty) treated boys also achieved their genetic target height. Predictions based on the Bayley-Pinneau method at Tanner stage 3 for all boys and at discontinuation of therapy for treated boys overestimated the achieved final height (P < 0.001). In conclusion, boys with sexual precocity, whether central precocious puberty or early puberty, may have either accelerated or slow pubertal development. The decision to institute suppressive therapy should be based also on the rate of pubertal progression. Treatment should be offered only to those (either central precocious puberty or early puberty) with accelerated growth and bone maturation rates and rapid increase in T levels. Suppression therapy apparently converts accelerated puberty into nonsustained slow puberty and probably prevents compromised final height.

Body Height↗

PubMed2000

Acceleration of trophoblast differentiation by heparin-binding EGF-like growth factor is dependent on the stage-specific activation of calcium influx by ErbB receptors in developing mouse blastocysts.

Heparin-binding EGF-like growth factor (HB-EGF) is expressed in the mouse endometrial epithelium during implantation exclusively at sites apposed to embryos and accelerates the development of cultured blastocysts, suggesting that it may regulate peri-implantation development in utero. We have examined the influence of HB-EGF on mouse trophoblast differentiation in vitro and the associated intracellular signaling pathways. HB-EGF both induced intracellular Ca2+ signaling and accelerated trophoblast development to an adhesion-competent stage, but only late on gestation day 4 after ErbB4, a receptor for HB-EGF, translocated from the cytoplasm to the apical surface of trophoblast cells. The acceleration of blastocyst differentiation by HB-EGF was attenuated after inhibition of protein tyrosine kinase activity or removal of surface heparan sulfate, as expected. Chelation of intracellular Ca2+ blocked the ability of HB-EGF to accelerate development, as did inhibitors of protein kinase C or calmodulin. The absence of any effect by a phospholipase C inhibitor and the requirement for extracellular Ca2+ suggested that the accrued free cytoplasmic Ca2+ did not originate from inositol phosphate-sensitive intracellular stores, but through Ca2+ influx. Indeed, N-type Ca2+ channel blockers specifically inhibited the ability of HB-EGF to both induce Ca2+ signaling and accelerate trophoblast development. We conclude that HB-EGF accelerates the differentiation of trophoblast cells to an adhesion-competent stage by inducing Ca2+ influx, which activates calmodulin and protein kinase C. An upstream role for ErbB4 in this pathway is implicated by the timing of its translocation to the trophoblast surface.

Animals↗

PubMed1991

Effects of heart rate and pulmonary artery pressure on Doppler pulmonary artery acceleration time in experimental acute pulmonary hypertension.

Chronic pulmonary hypertension in humans is characterized by shortening of the pulmonary artery acceleration time as measured by Doppler echocardiography, such that the higher the pulmonary artery pressure, the shorter the pulmonary acceleration time. Increases in heart rate are also known to produce decreases in the pulmonary artery acceleration time. To explore the relationship between mean pulmonary artery pressure, heart rate, and Doppler pulmonary artery acceleration time, experimental acute pulmonary hypertension was created in nine Duroc swine, either by infusion of Sephadex beads with embolization of the pulmonary arterial circulation or by partially occluding the main pulmonary artery 8 to 10 cm distal to the pulmonic valve. Pulmonary artery Doppler flow velocity recordings and invasive pressure measurements were made at baseline and at paced atrial rates ranging from 60 to 160 beats per minute, in 20-beat increments. The results in this acute animal model reveal that increases in heart rate produced significant decreases in Doppler pulmonary artery acceleration time at mean pressures below 25 mm Hg. However, with mean pulmonary artery pressures greater than 25 mm Hg, both heart rate and increases in pulmonary artery pressure had no significant effect on acceleration time.

Acute Disease↗

PubMed2004

A comparative study of an accelerated life-test model and a toxicokinetics-based model for the analysis of Porcellio scaber survival data.

Statistical models have long been used for reliability analysis and risk assessment. In the present study, an accelerated life-test model was used to analyze a set of dose-time-response data obtained with the terrestrial isopod Porcellio scaber. Survival data were experimentally obtained by exposing P. scaber to diazinon (a nonpersistent insecticide) at six concentrations between 2 and 11.31 microg/g (toxicant/soil). Survival data are presented on a weekly basis. The accelerated life-test model assumed a log-normal distribution and constant variance across all diazinon concentrations. Model parameters were obtained by maximum likelihood estimation. The accelerated life-test model was compared to a toxicokinetics-based model reported in the literature. Survival predictions made by both models were compared with the observed data. Both the accelerated life-test model and the toxicokinetics-based model underestimated toxicity at a diazinon concentration of 8 microg/g. Overall, however, the accelerated life-test model outperformed the toxicokinetics-based model, with survival predictions closer to the observed data in most cases and a stronger correlation between predicted and observed survivals. However, as a statistical model, the accelerated life-test model did not reveal mechanistic information, and only statistical and distributional interpretations of its model parameters could be made.

Animals↗

PubMed2003

Accelerated chilling of carcasses to improve pork quality.

Our objectives were to determine the optimal accelerated chill time immediately postmortem necessary to improve the quality of pork muscle and to decrease the incidence of pale, soft, and exudative pork. Carcasses from 81 market hogs were cooled either by conventional chill (CC) at 2 degrees C or by accelerated chill (AC) at -32 degrees C for 60, 90, 120, or 150 min, and then placed into a 2 degrees C cooler for the remainder of the 24-h chill period. Loin muscle pH was higher (P < 0.05) for the carcasses that were accelerated chilled longer than 60 min. Although loin visual color, texture, and firmness scores increased (P < 0.05) with AC time, no improvements were noted beyond 60 min. Color, pH, texture, firmness, and CIE L*a*b* values of fresh ham muscles were not (P > 0.05) affected by AC. In addition, AC did not (P > 0.05) affect purge, drip, or thaw loss of fresh products, sensory scores of loins or processed hams (except initial juiciness; P < 0.05), water-holding capacity of processed hams, or processing characteristics of hams. Cooking loss and Warner-Bratzler shear values for hams and loins were not (P > 0.05) affected by AC. Accelerated chilling caused loins to be darker (lower L* value; P < 0.05) and to have lower (P < 0.05) b* values (less yellow) than CC loins. Accelerated chilling increased water-holding capacity in fresh hams, bound water being the greatest (P < 0.05) in the 120- and 150-min AC groups. These results demonstrate that improvements in pork loin quality can be made using freezer-accelerated chilling for carcasses.

Animals↗

PubMed2006

A profile of accelerated BSN graduates, 2004.

In 1971, Saint Louis University initiated a new type of baccalaureate nursing curriculum, the accelerated option. Since then, there has been an explosion of accelerated baccalaureate nursing (BSN) programs. Despite the popularity of these programs, there is little reported research on the type of students entering accelerated BSN programs and their degree of satisfaction with the programs. This descriptive study aimed to provide a profile of one graduating class of accelerated BSN students. Students in this study had a mean age of 28 and were most likely to have previous baccalaureate degrees in the physical or social sciences. Results indicated that students were, on the whole, satisfied with the accelerated BSN experience, but that the program does pose academic, financial, and personal challenges. Implications for recruitment and retention of accelerated BSN students are discussed.

Adaptation, Psychological↗

PubMed2000

A mechanism for IL-10-mediated diabetes in the nonobese diabetic (NOD) mouse: ICAM-1 deficiency blocks accelerated diabetes.

Neonatal islet-specific expression of IL-10 in nonobese diabetic (NOD) mice accelerates the onset of diabetes, whereas systemic treatment of young NOD mice with IL-10 prevents diabetes. The mechanism for acceleration of diabetes in IL-10-NOD mice is not known. Here we show, by adoptive transfers, that prediabetic or diabetic NOD splenocytes upon encountering IL-10 in the pancreatic islets readily promoted diabetes. This outcome suggests that the compartment of exposure, not the timing, confers proinflammatory effects on this molecule. Moreover, injection of IL-10-deficient NOD splenocytes into transgenic IL-10-NOD.scid/scid mice elicited accelerated disease, demonstrating that pancreatic IL-10 but not endogenous IL-10 is sufficient for the acceleration of diabetes. Immunohistochemical analysis revealed hyperexpression of ICAM-1 on the vascular endothelium of IL-10-NOD mice. The finding suggests that IL-10 may promote diabetes via an ICAM-1-dependent pathway. We found that introduction of ICAM-1 deficiency into IL-10-NOD mice as well as into NOD mice prevented accelerated insulitis and diabetes. Failure to develop insulitis and diabetes was preceded by the absence of GAD65-specific T cell responses. The data suggest that ICAM-1 plays a role in the formation of the "immunological synapse", thereby affecting the generation and/or expansion of islet-specific T cells. In addition, ICAM-1 also played a role in the effector phase of autoimmune diabetes because adoptive transfer of diabetogenic BDC2.5 T cells failed to elicit clinical disease in ICAM-1-deficient IL-10-NOD and NOD mice. These findings provide evidence that pancreatic IL-10 is sufficient to drive pathogenic autoimmune responses and accelerates diabetes via an ICAM-1-dependent pathway.

Adoptive Transfer↗

PubMedDate not supplied

Task dependent processing of visual information about target acceleration.

The objective of this study was to investigate the sensitivity of the perceptual and motor systems to target acceleration information using verbal magnitude estimations of target acceleration and manual interception of these targets. The results showed that in the perceptual task the participants were responding mainly to acceleration threshold values, which is acceleration as a function of initial, final, and average velocities, rather then to the absolute accelerations. When manually intercepting the targets the participants responded mainly to the absolute acceleration value and target initial velocity. Thus, these results suggest that target motion can be processed in the ventral (perception) and dorsal (action) visual streams however different motion characteristics are processed in these streams depending on the required output.

Adult↗

PubMed1987

Multiple receptors linked to inhibition of adenylate cyclase accelerate Na+/H+ exchange in neuroblastoma x glioma cells via a mechanism other than decreased cAMP accumulation.

alpha 2-Adrenergic receptors, a population of receptors linked to inhibition of adenylate cyclase, accelerate Na+/H+ exchange in NG108-15 neuroblastoma x glioma cells (Isom, L. L., Cragoe, E. J., Jr., and Limbird, L. E. (1987) J. Biol. Chem. 262, 6750-6757). We now report that two other receptor populations linked to inhibition of adenylate cyclase, muscarinic cholinergic and delta-opiate receptors, also alkalinize the interior of NG108-15 cells, as measured with the pH-sensitive fluorescent probe, 2,7-biscarboxyethyl-5(6)-carboxy-fluorescein. Manipulations that block Na+/H+ exchange, i.e. removal of extracellular Na+, reduction of extracellular pH to equal that of intracellular pH, and addition of 5-amino-substituted analogs of amiloride, all block alpha 2-adrenergic, delta-opiate, or muscarinic cholinergic receptor-induced alkalinization in a parallel fashion. These data suggest that all three populations of receptors alkalinize NG108-15 cells by acceleration of Na+/H+ exchange and do so via a shared or similar mechanism. Although these three receptor populations are linked to inhibition of adenylate cyclase, decreased production of cAMP does not appear to be the mechanism responsible for receptor-accelerated Na+/H+ exchange. Thus, ADP-ribosylation of intact NG108-15 cells with Bordetella pertussis islet-activating protein prevents attenuation of prostaglandin E1-stimulated cAMP accumulation by alpha 2-adrenergic, muscarinic, and delta-opiate agonists but has no measurable effect on the ability of these agonists to accelerate Na+/H+ exchange. Similarly, manipulations that block receptor-accelerated Na+/H+ exchange influence but do not block receptor-mediated attenuation of cAMP accumulation. Thus, the present data suggest that these two receptor-mediated biochemical events, acceleration of Na+/H+ exchange and attenuation of cAMP accumulation, occur through divergent mechanisms in NG108-15 cells.

Adenosine Diphosphate Ribose↗

PubMed1985

Relationship between accelerations and decelerations in heart rate and skeletal muscle activity in fetal sheep.

Accelerations in fetal heart rate have been shown to be closely related to fetal body movements and are indicative of well-being in the human fetus. We have examined the association of accelerations and decelerations in heart rate with skeletal muscle activity in 8 fetal sheep between 125 and 145 days' gestation. Accelerations/decelerations were defined as transient increases/decreases in fetal heart rate of greater than or equal to 10 beats/min. lasting for 5 s or longer. For accelerations (n = 1180), the mean duration was 18.8 +/- 1.5 s (SEM) and the mean amplitude was 25.3 +/- 1.2 beats/min; for decelerations (n = 237), the mean duration was 17.4 +/- 1.6 s and the mean amplitude was 18.7 +/- 1.0 beats/min. Electromyograms were recorded from the nuchal muscles and antagonistic muscle groups of the fetal forelimb and hindlimb. Electromyogram activity occurred during 88.4 +/- 2.8% of accelerations and 60.6 +/- 7.7% of decelerations. There was a 36.6% reduction in the number of accelerations following fetal paralysis with gallamine, but no change in their amplitude or duration. It is concluded that accelerations in heart rate are highly associated with skeletal muscle activity in fetal sheep. The majority of these occur as a result of central neuronal output rather than as a consequence of fetal movement.

Animals↗

PubMed1976

Cellular and humorial immune responses in mice. III. Acceleration of delayed hypersensitivity response by presensitization with suboptimal dose of antigen.

Delayed hypersensitivity (DH) response in mice induced by subcutaneous (s.c.) injection of optimal dose of sheep red blood cells (SRBC) 10(8)) was accelerated by s.c. injection of the antigen of 10(3) or more doses, given 2 or more days earlier. The accelerated response appeared soon after the injection of optimal antigen dose, that is, 1 or 2 days earlier than the response of non-presensitized control. The acceleration was antigen specific. The accelerated response was generally accompanied by an acceleration and/or enhancement of humoral antibody response. Parallel to the acceleration of DH response, the proliferation of regional lymph node cells in the presensitized mice was induced immediately after the following injection of 10(8) SRBC, 1 day earlier than that of non-presensitized animals. These results suggest that presensitization of mice with the antigen induces DH-related memory cells which proliferate immediately after the following injection and function as effector cells for DH reactions, and that the development of DH-related memory cells occurs in close relation to that of helper thymus-derived (T) cells for antibody production.

Animals↗

PubMed1984

Pentobarbital antagonizes the effect of morphine on cardiac acceleration response to noxious stimulation.

The effects of morphine alone and in combination with pentobarbital on the cardiac acceleration response to somatic noxious stimulation were studied in 145 rats. It was found that pentobarbital in subanesthetic doses (1-10 mg X kg-1) weakened the inhibitory effect of morphine on the cardiac acceleration response; it antagonized the effect of morphine in a dose-dependent manner. The maximal antagonism was observed with a pentobarbital dose of 10 mg X kg-1. With this dose of pentobarbital, even 200 mg X kg-1 or morphine was unable to block the cardiac acceleration response (without pentobarbital, morphine blocked the response in a dose of 10 mg X kg-1). Caffeine (10 mg X kg-1), on the contrary, strengthened the effect of morphine on the cardiac acceleration response: there was a significant (P less than 0.05) shift to the left along the dose axis in the position of morphine dose-effect curve for the cardiac acceleration response. It has been suggested that the effect of morphine on the cardiac acceleration response to noxious stimulation results primarily from activation of inhibitory control mechanisms concerned with this response; pentobarbital depresses the inhibitory control mechanisms and, therefore, weakens the effect of morphine.

Animals↗

PubMed1980

Cigarettes and accelerated hypertension.

The smoking and drinking habits of 58 patients with accelerated hypertension were compared with those of a control group of 58 patients with benign hypertension, each individually matched for age, sex and date of presentation. Thirty-eight (66 percent) of the patients with accelerated hypertension were regular smokers compared to 26 (45 percent) of the control group. This excess of smokers was significant, but the average number of cigarettes smoked by smokers in the two groups was similar. The number of patients known to consume alcohol was the same in the two groups; and there were no significant differences in amount of alcohol drunk. Smoking and alcohol habits were not related. Thirty-six patients (62 percent) with accelerated hypertension had serum creatinine levels greater than 0.12 mmol/l compared with nine (16 percent) of the control group. Seventeen (29 percent) patients with accelerated hypertension were known to have died compared with five (9 percent) of the control group. This survey confirms that, as shown by recent studies in Britain, smoking is more common in patients presenting with accelerated than with benign hypertension. It appears that hypertensive patients who smoke regularly are more likely to develop the accelerated phase than those who do not.

Alcohol Drinking↗

PubMedDate not supplied

Influence of graft rejection on incidence of accelerated graft coronary artery disease: a new approach to analysis.

Conflicting data exist on the role of graft rejection as a risk factor for later development of accelerated graft coronary artery disease. We analyzed 126 consecutive heart transplant recipients treated with cyclosporine-based immunosuppressive regimens and devised an arbitrary method to incorporate the number, duration, and severity of myocardial rejection episodes during the first postoperative year, resulting in a rejection score for each patient. We then correlated the later incidence (mean follow-up, 4 years) of angiographic accelerated graft coronary artery disease with this rejection score and with its components: number, duration, and severity of rejection; number and duration of untreated rejection; and incidence and duration of delayed rejection therapy. Accelerated graft coronary artery disease developed in 60 patients (48%). The rejection score was 96.7 for patients in the "no accelerated graft coronary artery disease" group and 110.4 for those in the "accelerated graft coronary artery disease" group (p = NS). No significant difference was noted between patients with and without disease in any of the other seven rejection parameters analyzed, and no significant difference in time to occurrence of disease was noted between groups divided at the median rejection score. Donor age was older and fasting triglyceride blood level was higher in patients with accelerated graft coronary artery disease than in those without disease. All other clinical characteristics, including HLA mismatches, ischemic time, blood pressure, lipid profile, and drug therapy, did not differ between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1977

Fetal heart rate acceleration in relation to the oxytocin challenge test.

Fetal heart rate (FHR) acceleration was evaluated in 1570 oxytocin challenge test (OCT) results, which were performed on 565 high-risk patients. In positive OCTs a significant decrease or lack of FHR acceleration was noted. Fetuses with positive OCTs and lack of FHR acceleration were more compromised than those with better FHR acceleration.. Negative OCTs were associated with a good FHR acceleration approximately 95% of the time. Study of FHR acceleration in suspicious OCTs proved to be helpful in determining the significance and prognosis of a suspicious OCT.

Adult↗

PubMedDate not supplied

Does cyclosporin A have any effect on accelerated atherosclerosis in absence of graft rejection? Pathologic and morphometric evaluation in an experimental model.

BACKGROUND: The effects of cyclosporin A on accelerated atherosclerosis were studied in an experimental model of aortic isotransplantation. METHODS: Seventy-six Lewis rats were studied. Forty-one abdominal aortic isografts were performed and divided into five groups: 2-day isografts and 15- and 100-day isografts with and without cyclosporin treatment. The remaining rats were divided into seven groups: 15- and 100-day sham-operated, with and without cyclosporin administration; 15- and 100-day animals with cyclosporin treatment only; and normal controls. Cyclosporin was injected subcutaneously in doses of 10 mg/kg daily for the first 15 days and afterward every other day. Longitudinal sections of the proximal anastomosis and cross sections of the midgraft region were measured with a semiautomatic image-analyzer. RESULTS: Histologic analysis showed that accelerated atherosclerosis was not observed either in NT2 rats or in nontransplanted animals. In the 15-day isografts, accelerated atherosclerosis was present in the perianastomotic tract of the recipient aorta in nine of nine NT15 rats, whereas it was found only in three of nine T15 animals (p < 0.02). Histomorphometric analysis showed that accelerated atherosclerosis was less pronounced in the T100 isografts than in the NT100 ones, this difference being significant at the recipient anastomotic side only (p < 0.0005). CONCLUSIONS: The present results support the hypothesis that cyclosporin, at immunosuppressant and nontoxic doses, can delay the onset and progression of accelerated atherosclerosis and that its effects are more significant at the recipient side of the anastomosis where accelerated atherosclerosis begins to develop.

Anastomosis, Surgical↗

PubMedDate not supplied

Effects of calcium channel blockers on impairment of brain function in senescence-accelerated mice.

The effects of the L-type calcium channel blockers, nicardipine, nimodipine, nilvadipine and amlodipine, on brain dysfunction were examined in senescence-accelerated-prone mice. A disturbed brain function in passive avoidance response, forced swimming, rota-rod and traction tests was observed in senescence-accelerated-prone mice compared to senescence-accelerated-resistant mice. A single oral administration of the four calcium channel blockers tested had little effect on the brain dysfunction in senescence-accelerated-prone mice. In contrast, the daily oral administration of nicardipine (1 and 3 mg/kg), nimodipine (3 mg/kg) and nilvadipine (3 mg/kg), once a day for three weeks, prolonged the shortened latency of step-through in the passive avoidance response and falling time in rota-rod tests. Brain dysfunction in forced swimming and traction tests was not influenced by repeated administration of these blockers. Repeated administration of amlodipine for three weeks in senescence-accelerated-prone mice showed little pharmacological actions in all four tests. Thus, we found that repeated administration of nicardipine, nimodipine and nilvadipine ameliorated the brain dysfunction in these mice. Furthermore, the present study suggests that senescence-accelerated-prone mice can be used as an appropriate model for evaluating the pharmacological effects of calcium channel blockers on brain dysfunction.

Amlodipine↗

PubMed1997

Expression of human decay accelerating factor may protect pig lung from hyperacute rejection by human blood.

BACKGROUND: Hyperacute rejection currently prevents clinical application of discordant lung xenografts. Pigs transgenic for human regulators of complement activation offer one promising potential solution to this problem. METHODS: Using fresh human blood in an ex vivo lung perfusion model, we studied eight different strains of pigs transgenic for human decay accelerating factor. Survival (by blood flow and gas transfer criteria) were correlated with immunohistologic evidence of pulmonary human decay accelerating factor expression and complement activation. RESULTS: With human blood perfusion, blood flow through the unmodified pig lung rapidly falls and is not restored by continuous infusion or high-dose bolus of prostacyclin. Airway pressure also rises rapidly and is followed promptly by loss of gas transfer. Four of the transgenic pig strains showed no difference from this pattern. Immunohistochemistry for human decay accelerating factor revealed low or no pulmonary expression in these lungs. In contrast, two of five transgenic pig lungs that had significant decay accelerating factor expression demonstrated recovery of pulmonary blood flow within 1 hour, and rejection was delayed, from less than 20 minutes in controls to about 1 hour. Complement activation, particularly the alternative pathway, was inhibited in lungs with high levels of endothelial decay accelerating factor expression. CONCLUSIONS: Lungs from some strains of pig transgenic for human decay accelerating factor demonstrate incomplete physiologic and histologic protection from hyperacute rejection. Although complement-independent pathogenic mechanisms may present a formidable obstacle, pig lungs transgenic for human complement regulatory proteins may facilitate discordant lung transplantation in human beings.

Animals↗