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PubMed1988

Growth hormone and insulin-like growth factor-I accelerate PMSG-induced differentiation of granulosa cells.

To investigate the nature of the interactions between growth hormone (GH), insulin-like growth factor-I (IGF-I) and follicle stimulating hormone (FSH), their temporal and dose-related effects on steroidogenesis were studied in granulosa cells from stilboestrol-treated immature rats, stimulated in vitro with pregnant mare's serum gonadotropin (PMSG) or FSH. GH in the presence of PMSG enhanced aromatase activity and progesterone synthesis above that induced by maximally stimulating doses of PMSG alone, and accelerated PMSG-induced peak levels for both progesterone and aromatase activity. IGF-I also enhanced PMSG-induced aromatase activity and progesterone production, and accelerated their peak responses in a similar fashion to the effects observed for GH. The stimulatory actions of IGF-I could still be observed after the removal of FSH from the cultures, and appeared to be partly independent of cAMP. It is concluded that both GH and IGF-I act on FSH-induced granulosa cells to accelerate the differentiation of the follicular cell to a lutein cell.

Animals↗

PubMed1996

Evidence that glucose metabolism is decreased in the cerebrum of aged female senescence-accelerated mouse; possible involvement of a low hexokinase activity.

d-Glucose metabolism in cerebral cells prepared from aged senescence-accelerated mouse (SAM), was investigated in consideration of a sex difference. The production of 14CO2 from 6-[14C]D-glucose was reduced in female senescence-accelerated-prone mouse (SAMP) 8, a prone substrain, in comparison with that in female senescence-accelerated-resistant mouse (SAMR) 2, a control substrain, whereas there was no difference in males. The 2-deoxy-D-glucose uptake into cerebral cells from female SAMP8 was also lower than that of control mice. But, the 3-O-methyl-D-glucose uptake in SAMP8 was higher than that of SAMR2, suggesting that the low hexokinase activity was involved in the decreased glucose metabolism in cerebrum of SAMP8 females irrespective of glucose transporter. This possibility was supported by the finding that the contents of glucose 6-phosphate produced from glucose added to cerebral cells from SAMP8 was lower than that in ICR mice.

3-O-Methylglucose↗

PubMed1980

The heparin-accelerated neutralisation of bovine alpha and beta thrombins by antithrombin III.

The heparin-accelerated neutralisation of bovine alpha and beta thrombins has been examined using a peptide substrate H-D-phenylalanyl-pipecolyl-arginine-paranitroanilide-HCl to measure thrombin amidase activity. Alpha and beta thrombins were both neutralised by antithrombin III and this neutralisation was further accelerated by the presence of small amounts of heparin. Low and high molecular weight heparin and heparins fractionated by their affinity for antithrombin III were all able to accelerate the neutralisation of alpha and beta thrombin. This work is therefore unable to confirm reports that alpha and beta thrombins have different heparin sensitivities.

Animals↗

PubMed1995

Excess EDRF/NO, a potentially deleterious condition that may be involved in accelerated atherogenesis and other chronic disease states.

1. To date, no method exists for preventing the injury-induced, accelerated atherogenesis that can occur as a "late complication" after initially successful invasive cardiovascular therapy (e.g. coronary angioplasty, endarterectomy). The problems intrinsic to some of the therapeutic approaches that are presently being developed have been analyzed, and the need for an alternative approach is evident. 2. An hypothesis is advanced, providing a novel conceptual basis for developing preventive therapy for accelerated atherogenesis, as well as for other chronic (degenerative) disease states, using agents that selectively inhibit the actions and metabolic transformations of excessive amounts of endogenously-derived and/or exogenously-acquired nitric oxide (NO). 3. It is considered that excess NO can damage tissue by enhancing the formation of hydroxyl radicals (OH.) via the peroxynitrite pathway and alpha-hydroxynitrosamines via nitrosation processes, and that it can stimulate cell proliferation by activating guanyl cyclase. These actions would facilitate the process of accelerated atherogenesis. 4. Selectivity for opposing the effects and metabolic handling of excess NO, regardless of its origin (endogenous via the action of constitutive or inducible NO synthase, or exogenous), rather than selectivity for inhibiting the activity of inducible versus constitutive NO synthase, is considered to be the key element required of candidate therapeutic agents. 5. The vitamin C derivative, 2-O-octadecylascorbic acid, which could protect that part of the NO mechanism that is essential for normal function by scavenging superoxide anion-radicals (O2-., while preventing the formation of OH. and potentially toxic nitrosamines via metabolic reactions involving excess NO, represents a model compound for developing effective therapy.

Animals↗

PubMed1988

Effects of accelerated fractionation on radiation injury of the small intestine: a new rat model.

The present study assessed the influence of shortening the overall treatment time (accelerated fractionation) on radiation injury of the small intestine. A rat model which allowed repeated irradiation of a localized segment of small intestine was developed. Young adult male Sprague-Dawley rats were orchiectomized, and a loop of the distal ileum was transposed to the left part of the scrotum. The intestinal segment was irradiated with a total dose of 56 Gy, given in 20 fractions, the total treatment time being either 26, 12, or 7 days (i.e. 1, 2, or 3 fractions per day). Radiation injury was assessed by histopathologic examination at 6 hr and at 2 weeks after the last irradiation. The surgical procedure was without complications. Shortening the overall treatment time by giving more than one radiation dose per day resulted in markedly increased injury both at 6 hr and at 2 weeks. It is concluded that accelerated fractionation results in increased radiation injury of the intestine when compared with standard fractionation. Because there may be a relationship between early and late effects in the intestine, our results also indicate that increased late radiation enteropathy may result from accelerated fractionation.

Animals↗

PubMed1993

Measurement of mechanical accuracy of isocenter in conventional linear-accelerator-based radiosurgery.

PURPOSE: Five Varian linear accelerators were studied to determine whether their mechanical isocentric accuracies were sufficient for radiosurgery and, if not, if the observed errors were sufficiently consistent and predictable to be correctable by some form of secondary collimator steering device to maintain isocentric alignment. METHODS AND MATERIALS: A 0.3 mW 670 nm diode laser was mounted in the secondary collimator insert of a radiosurgery extended collimator assembly. A cylindrical lens was used to create a laser fan beam that passed through isocenter and could be oriented parallel or perpendicular to the plane of rotation. A position sensitive photo-diode having an electrical output that varied with the portion of its surface illuminated was mounted at isocenter in a rotational mount. This mount tracked the accelerator gantry such that the surface of the photo-diode remained perpendicular to the laser beam during gantry rotation. An X/Y recorder was connected to the gantry-angle potentiometer of the accelerator and to the photo-diode and plotted the positional variation from isocenter with gantry rotation. RESULTS: The root-mean-square error for the five machines was +/- 0.06 to +/- 0.08 mm in the plane of rotation and +/- 0.17 to +/- 0.35 mm out of (perpendicular to) the plane of rotation. The in-plane-of-rotation errors tended to be maximal near the diagonal gantry angles and the out-of-plane-of-rotation errors were maximal in the over and under vertical positions. CONCLUSIONS: Both types of errors were predictable but only the out-of-plane-of-rotation errors were considered large enough to warrant consideration of correction (although the need is debatable). On all the tested machines, the out-of-plane-of-rotation error curve was a relatively smooth bell-shaped function that would be readily amenable to correction. The diode laser/photo-detector system used should prove useful in accurately defining isocenter and facilitating the precise adjustment of the laser isocenter lights.

Humans↗

PubMed1993

A phase I/II study to evaluate accelerated fractionation via concomitant boost for squamous, adeno, and large cell carcinoma of the lung: report of Radiation Therapy Oncology Group 84-07.

PURPOSE: A Phase I/II trial was conducted by the Radiation Therapy Oncology Group from 1984 to 1989 for 355 evaluable patients with non-small-cell lung cancer to assess tolerance to and efficacy of accelerated fractionation irradiation via concomitant boost. METHODS AND MATERIALS: "Large" fields (primary tumor and locoregional lymph nodes) received 1.8 Gy followed after 4 to 6 hr by 1.8 Gy two to three times weekly to reduced "boost" fields (primary and involved nodes only). The total doses escalated during the study and started with 63 Gy in 5 weeks (45 Gy "large" field and 18 Gy "boost") for 61 patients. After follow-up for ongoing toxicity assessment, the total dose was increased to 70.2 Gy in 5.5 weeks (50.4 Gy "large" field and 19.8 Gy "boost") for the next 180 patients. The last 114 patients received 70.2 Gy in 5 weeks (45 Gy "large" field and 25.2 Gy "boost"). RESULTS: Pretreatment patient characteristics were well balanced between the three treatment arms. Grade 3 acute toxicity was 7% for the 63 Gy arm; it was 14% and 17% for the two 70 Gy arms. Grade 4 or greater acute toxicities (esophagitis and pneumonitis) were 2 to 3% for all three arms. Late toxicities ranged between 5 and 9% (> or = Grade 3) and 0 to 2% (> or = Grade 4), not statistically different among the three arms. There was no difference between the three regimens in median survival (9 months) or 1-year survival (39 to 44%). However, the 2-year survivals ranged from 16% (63 Gy) to 21% ("shortened" 70.2 Gy). Among 176 patients who had the same criteria as Cancer and Leukemia Group B protocol 84-33 (American Joint Committee on Cancer Staging, 1984, Stage III; Karnofsky performance status 70 to 100; < 6% weight loss), the 2-year survival rates ranged from 18 to 22%. CONCLUSION: Concomitant boost accelerated fractionation irradiation regimens for non-small cell lung cancer may offer improved long-term survival without enhanced late toxicity. While acute toxicity is somewhat increased, further refinement of the relationship of "large" to "boost" field doses may improve the therapeutic ratio. Further Phase I/II testing seems justified and necessary, before concomitant boost accelerated fractionation irradiation is tested in Phase III trials for NSCLC.

Adenocarcinoma↗

PubMed1994

Accelerated radiation therapy in the treatment of very advanced and inoperable head and neck cancers.

PURPOSE: A Phase II trial testing a continuous and accelerated regimen of radiotherapy in very advanced head and neck cancers. METHODS AND MATERIALS: From 1988 to 1990, 47 patients with very advanced and inoperable tumors (38/47 T4) of the oral cavity and the oropharynx were submitted to a continuous and accelerated regimen of hyperfractionated radiation therapy: three daily fractions of 0.9 Gy were delivered 5 days-a-week, up to the 70 Gy total dose, reducing the overall treatment time to 5.5 weeks. RESULTS: Immediate tolerance was good: only 56% of the patients experienced a Grade 3 mucositis, and the mean weight loss was 2 kg. The 2-year survival rate was 24.6%. The 2-year local control rate was 42.6%, which compares favorably with the 20% local control rate obtained in a historical control group of patients treated with another hyperfractionated regimen between 1978 and 1986. Mid- and long-term tolerance were excellent, no late complication or sequellae were observed which was also quite different from our previous experience. CONCLUSION: These results suggest an improvement of the local control and the therapeutic ratio with acceleration of radiotherapy in head and neck cancers.

Adult↗

PubMed1996

Vestibulo-ocular reflex of the squirrel monkey during eccentric rotation with centripetal acceleration along the naso-occipital axis.

The vestibulo-ocular reflexes (VOR) are determined not only by angular acceleration, but also by the presence of gravity and linear acceleration. This phenomenon was studied by measuring three-dimensional nystagmic eye movements, with implanted search coils, in four male squirrel monkeys. Monkeys were rotated in the dark at 200 degrees/s, centrally or 79 cm off-axis, with the axis of rotation always aligned with gravity and the spinal axis of the upright monkeys. The monkey's position relative to the centripetal acceleration (facing center or back to center) had a dramatic influence on the VOR. These studies show that a torsional response was always elicited that acted to shift the axis of eye rotation toward alignment with gravito-inertial force. On the other hand, a slow phase downward vertical response usually existed, which shifted the axis of eye rotation away from the gravito-inertial force. These findings were consistent across all monkeys. In another set of tests, the same monkeys were rapidly tilted about their interaural (pitch) axis. Tilt orientations of 45 degrees and 90 degrees were maintained for 1 min. Other than a compensatory angular VOR during the rotation, no consistent eye velocity response was ever observed during or following the tilt. The absence of any response following tilt proves that the observed torsional and vertical responses were not a positional nystagmus. Model simulations qualitatively predict all components of these eccentric rotation and tilt responses. These simulations support the conclusion that the VOR during eccentric rotation may consist of two components: a linear VOR and a rotational VOR. The model predicts a slow phase downward, vertical, linear VOR during eccentric rotation even though there was never a change in the force aligned with monkey's spinal (Z) axis. The model also predicts the torsional components of the response that shift the rotation axis of the angular VOR toward alignment with gravito-inertial force.

Animals↗

PubMed1990

Syndromes of accelerated atherosclerosis: role of vascular injury and smooth muscle cell proliferation.

Vascular injury represents a critical initiating event in the pathogenesis of various vascular diseases, including atherosclerosis. This review discusses 1) the current understanding and a new pathologic classification of vascular injury; 2) the resultant cellular pathophysiologic responses, specifically, lipid accumulation, platelet aggregation, thrombus formation and smooth muscle cell proliferation; 3) the role of vascular injury in the pathogenesis of spontaneous and accelerated atherosclerosis; and 4) emerging therapeutic approaches in preventing these vascular diseases. The process of type I vascular injury (nondenuding functional injury) followed by lipid accumulation, monocyte and platelet adhesion, smooth muscle cell proliferation and resultant plaque formation represents the prevalent view of the early stages of spontaneous atherogenesis. The syndromes of accelerated atherosclerosis (namely, heart transplant atherosclerosis, coronary vein graft disease and restenosis after percutaneous transluminal coronary angioplasty) appear to share etiologic mechanisms with spontaneous atherosclerosis by means of the "response to injury" hypothesis. However, type II and type III vascular injury (denuding endothelial and intimal injury with or without medial damage) followed by thrombus and its organization by smooth muscle cell proliferation and subsequent fibrosis appear to be responsible for the vascular process. This accelerated and premature occlusive process accounts for significant morbidity and mortality in patients with these conditions. Better understanding of the nature of vascular injury and its pathophysiologic responses in these clinical situations may aid in developing therapeutic strategies for preventing these vascular diseases.

Animals↗

PubMed1995

Nature of flow acceleration into a finite-sized orifice: steady and pulsatile flow studies on the flow convergence region using simultaneous ultrasound Doppler flow mapping and laser Doppler velocimetry.

OBJECTIVES: This study investigated the proximal centerline flow convergence region simultaneously by both color Doppler and laser Doppler velocimetry. BACKGROUND: Although numerous investigations have been performed to test the flow convergence method, to our knowledge there has yet been no experimental study using reference standard velocimetric techniques to define precisely the hydrodynamic factors involved in the accelerating flow region during steady and pulsatile flow. METHODS: Using an in vitro model that allows velocity measurements by laser Doppler velocimetry with simultaneous comparison with color Doppler results, we studied the centerline flow acceleration region proximal to orifices of various sizes (0.08 to 2.0 cm2). RESULTS: Agreement between theory and experimental velocities was good for large flow rates through small orifices only, and only at distances > 1.2 cm from the orifice. Changing the orifice shape from circular to slitlike produced no significant changes in velocity profiles. Constraining the proximal side walls caused a significant increase in proximal velocities at distances > 0.7 cm for the largest orifice only (2.0 cm2). Calculated flow rates agreed well with actual flow rates, with functional dependence on proximal distance and orifice size. Velocity profiles for pulsatile flow were similar to steady state flow profiles and could be integrated to calculate stroke volumes, which followed actual flow volumes well, although with general overestimation (y = 1.22x + 0.164, r = 0.92), most likely due to the use of all available proximal velocities. CONCLUSIONS: The accelerating proximal flow region responds to several hydrodynamic factors that can affect flow quantitation using the flow convergence method in the clinical situation.

Blood Flow Velocity↗

PubMed1996

Evaluation of aortic regurgitation with digitally determined color Doppler-imaged flow convergence acceleration: a quantitative study in sheep.

OBJECTIVES: The aim of the present study was to validate a digital color Doppler-based centerline velocity/distance acceleration profile method for evaluating the severity of aortic regurgitation. BACKGROUND: Clinical and in vivo experimental applications of the flow convergence axial centerline velocity/distance profile method have recently been used to estimate regurgitant flow rates and regurgitant volumes in the presence of mitral regurgitation. METHODS: In six sheep, a total of 19 hemodynamic states were obtained pharmacologically 14 weeks after the original operation in which a portion of the aortic noncoronary (n = 3) or right coronary (n = 3) leaflet was excised to produce aortic regurgitation. Echocardiographic studies were performed to obtain complete proximal axial flow acceleration velocity/distance profiles during the time of peak regurgitant flow (usually early in diastole) for each hemodynamic state. For each steady state, the severity of aortic regurgitation was assessed by measurement of the magnitude of the regurgitant flow volume/beat, regurgitant fraction and instantaneous regurgitant flow rates determined by using both aortic and pulmonary artery electromagnetic flow probes. RESULTS: Grade I regurgitation (regurgitant volume/beat < 15 ml, six conditions), grade II regurgitation (regurgitant volume/beat between 16 ml and 30 ml, five conditions) and grade III-IV regurgitation (regurgitant volume/beat > 30 ml, eight conditions) were clearly separated by using the color Doppler centerline velocity/distance profile domain technique. Additionally, an equation for correlating "a" (the coefficient from the multiplicative curve fit for the velocity/distance relation) with the peak regurgitant flow rates (Q [liters/min]) was derived showing a high correlation between calculated peak flow rates by the color Doppler method and the actual peak flow rates (Q = 13a + 1.0, r = 0.95, p < 0.0001, SEE = 0.76 liters/min). CONCLUSIONS: This study, using quantified aortic regurgitation, demonstrates that the flow convergence axial centerline velocity/distance acceleration profile method can be used to evaluate the severity of aortic regurgitation.

Animals↗

PubMed1991

Acceleration of purine synthesis in mouse liver by glycogenolytic hormones.

Administration (ip) into fed mice of glucagon, epinephrine, vasopressin, oxytocin, angiotensin II, and dibutyryl cyclic AMP (dbcAMP) resulted in a rapid (within 2.5 to 15 min) elevation of PRPP content (two- to threefold) and in acceleration of the rate of de novo purine synthesis (twofold). Inhibition of the epinephrine-stimulated glycogenolysis by 2,5-anhydromannitol diminished markedly the acceleration effect of the hormone on the rate of purine synthesis. Administration of the hormones caused a rapid rise in the liver content of glucose 6-phosphate (G6P) by 15-70% but did not increase the ribose 5-phosphate (R5P) content. Liver ATP content was not affected. The hormones did not cause direct activation of PRPP synthetase, as gauged by the specific activity of the enzyme, its Km for substrates R5P and ATP, and its sensitivity to inhibition by ADP and GDP. The hormones did not increase the liver content of the enzyme activators Pi and Mg2+. The results suggest that the glycogenolytic hormones accelerate purine synthesis by a metabolic mechanism associated with the enhancement of glycogenolysis. PRPP synthesis is probably enhanced by the glycogenolysis-induced alterations in the cellular content of some metabolites other than R5P.

Animals↗

PubMed2004

Effects of an active accelerator pedal on driver behaviour and traffic safety after long-term use in urban areas.

The long-term effects of the active accelerator pedal (AAP) were evaluated in the city of Lund in 2000 and 2001. The system, installed in 284 vehicles, produced a counterforce in the accelerator pedal at the speed limit. It could, however be overridden by pressing the accelerator pedal harder. The results showed that test drivers' compliance with the speed limits improved considerably. Reduction in average speeds and less speed variation by the test vehicles indicate a great traffic-safety potential. Travel times were unaffected, while emission volumes decreased significantly.

Accidents, Traffic↗

PubMed2005

A study of neutron spectra from medical linear accelerators.

Medical accelerators with photon energies over 10 MeV generate an undesired fast neutron contamination in the therapeutic beam. In this work, the Monte Carlo code MCNP was used to simulate the transport of these photoneutrons across the head of various medical accelerators of high energy. The average and most probable neutron energies were obtained from these spectra, before and after crossing the accelerator shielding. The degradation of these spectra, when they cross concrete barriers with thickness which vary between 25 and 100 cm, was also studied.

Artifacts↗

PubMed2003

Physical stress by magnetic force accelerates differentiation of human osteoblasts.

We examined the effect of magnetic force on differentiation of cultured human osteoblasts. Magnetic microparticles (MPs) were introduced into the cytoplasm of a human osteoblast cell line and the cells were cultured in a magnetic field (MF) in group MP-MF. Three groups of controls were used: cells without MPs were cultured out of MF (group C), cells without MPs were cultured in MF (group MF), and cells with MPs were cultured out of MF (group MP). The cells in group MP-MF became larger and were elongated along the axis of the magnetic poles. Appearance of alkaline phosphatase (AlPase) activity, formation of bone nodules, and calcium deposition were accelerated depending on the intensity of the magnetic field. It takes longer culture in the other three groups to exhibit these changes. Core-binding factor A1 (Cbfa1: transcription factor for osteoblast differentiation) and osteocalcin (a bone-matrix protein involved in controlling osteogenesis) were expressed earlier or stronger in group MP-MF than the other groups. Then we compared phosphorylation of mitogen-activated protein kinase (MAPK) between group MP-MF and group C. Phosphorylation of p38(MAPK) (p38) was increased in group MP-MF, while total p38 as well as total and phosphorylated forms of MAPK/ERK 1/2 and SAPK/JNK were not changed between the two groups. When a p38 inhibitor, SB 203580, was added to the culture medium in group C, AlPase activity, formation of bone nodules, and calcium deposits were completely inhibited. On the other hand, they were inhibited only partially by a MAPK/ERK 1/2 inhibitor, U-0126. Based on these results, it is concluded that (1) osteoblast differentiation is accelerated by a magnetic force, (2) this acceleration is mainly attributed to the activation of p38 phosphorylation, and (3) the stimulus induced by a magnetic field offers a new approach to osteoblast differentiation.

Calcification, Physiologic↗

PubMed2006

Scrapie infection activates the replication of ecotropic, xenotropic, and polytropic murine leukemia virus (MuLV) in brains and spinal cords of senescence-accelerated mice: implication of MuLV in progression of scrapie pathogenesis.

Senescence-accelerated mice (SAMP8) have a short life span, whereas SAMR1 mice are resistant to accelerated senescence. Previously it has been reported that the Akv strain of ecotropic murine leukemia virus (E-MuLV) was detected in brains of SAMP8 mice but not in brains of SAMR1 mice. In order to determine the change of MuLV levels following scrapie infection, we analyzed the E-MuLV titer and the RNA expression levels of E-MuLV, xenotropic MuLV, and polytropic MuLV in brains and spinal cords of scrapie-infected SAM mice. The expression levels of the 3 types of MuLV were increased in scrapie-infected mice compared to control mice; E-MuLV expression was detected in infected SAMR1 mice, but only in the terminal stage of scrapie disease. We also examined incubation periods and the levels of PrPSc in scrapie-infected SAMR1 (sR1) and SAMP8 (sP8) mice. We confirmed that the incubation period was shorter in sP8 (210+/-5 days) compared to sR1 (235+/-10 days) after intraperitoneal injection. The levels of PrPSc in sP8 were significantly greater than sR1 at 210+/-5 days, but levels of PrPSc at the terminal stage of scrapie in both SAM strains were virtually identical. These results show the activation of MuLV expression by scrapie infection and suggest acceleration of the progression of scrapie pathogenesis by MuLV.

Animals↗

PubMed2006

EDEM1 regulates ER-associated degradation by accelerating de-mannosylation of folding-defective polypeptides and by inhibiting their covalent aggregation.

Proteins expressed in the endoplasmic reticulum (ER) are covalently modified by co-translational addition of pre-assembled core glycans (glucose(3)-mannose(9)-N-acetylglucosamine(2)) to asparagines in Asn-X-Ser/Thr motifs. N-Glycan processing is essential for protein quality control in the ER. Cleavages and re-additions of the innermost glucose residue prolong folding attempts in the calnexin cycle. Progressive loss of mannoses is a symptom of long retention in the ER and elicits preparation of terminally misfolded polypeptides for dislocation into the cytosol and proteasome-mediated degradation. The ER stress-induced protein EDEM1 regulates disposal of folding-defective glycoproteins and has been described as a mannose-binding lectin. Here we show that elevation of the intralumenal concentration of EDEM1 accelerates ER-associated degradation (ERAD) by accelerating de-mannosylation of terminally misfolded glycoproteins and by inhibiting formation of covalent aggregates upon release of terminally misfolded ERAD candidates from calnexin. Acceleration of Man(9) or Man(5)N-glycans dismantling upon overexpression was fully blocked by substitution in EDEM1 of one catalytic residue conserved amongst alpha1,2-mannosidases, thus suggesting that EDEM1 is an active mannosidase. This mutation did not affect the chaperone function of EDEM1.

Animals↗