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PubMed2004

Electrical stimulation accelerates and enhances expression of regeneration-associated genes in regenerating rat femoral motoneurons.

1. In this study we investigated whether electrical stimulation accelerates the upregulation of Talpha1-tubulin and GAP-43 (regeneration-associated genes; RAGs) and the downregulation of the medium-molecular-weight neurofilament (NFM), in concert with stimulation-induced acceleration of BDNF and trkB gene expression and axonal regeneration. 2. Two weeks prior to unilateral femoral nerve transection and suture, fluorogold (Fluorochrome Inc., Denver) or fluororuby (Dextran tetramethylrhodamine, Mol. Probes, D-1817, Eugene, OR) was injected into quadriceps muscles of the left and right hindlimbs to label the femoral motoneuron pools as previously described. Over a period of 7 days, fresh spinal cords were processed for semiquantitation of mRNA by using in situ hybridization. 3. There was an increase in Talpha1-tubulin and GAP-43 mRNA and a decline in the NFM mRNA at 7 days after nerve suture and sham stimulation but not in intact nerves. In contrast, 1-h stimulation of sutured but not intact nerves dramatically accelerated the changes in gene expression: mRNA levels of Talpha1-tubulin and GAP-43 were significantly elevated above control levels by 2 days while NFM mRNA was significantly reduced by 2 days in the sutured nerves. Thereby, the neurofilament/tubulin expression ratio was reduced at 2 days after suture and stimulation, possibly allowing more tubulin to be transported faster into the growing axons to accelerate the elongation rate following stimulation. Importantly, the changes in RAGs and NFM gene expression were delayed relative to the accelerated upregulation of BDNF and trkB mRNA by electrical stimulation. 4. The temporal sequence of upregulation of BDNF and trkB, altered gene expression of RAGs and NFM, and accelerated axonal outgrowth from the proximal nerve stump are consistent with a key role of BDNF and trkB in mediating the altered expression of RAGs and, in turn, the promotion of axonal outgrowth after electrical stimulation.

Animals↗

PubMed2006

Laser-plasma acceleration of quasi-monoenergetic protons from microstructured targets.

Particle acceleration based on high intensity laser systems (a process known as laser-plasma acceleration) has achieved high quality particle beams that compare favourably with conventional acceleration techniques in terms of emittance, brightness and pulse duration. A long-term difficulty associated with laser-plasma acceleration--the very broad, exponential energy spectrum of the emitted particles--has been overcome recently for electron beams. Here we report analogous results for ions, specifically the production of quasi-monoenergetic proton beams using laser-plasma accelerators. Reliable and reproducible laser-accelerated ion beams were achieved by intense laser irradiation of solid microstructured targets. This proof-of-principle experiment serves to illuminate the role of laser-generated plasmas as feasible particle sources. Scalability studies show that, owing to their compact size and reasonable cost, such table-top laser systems with high repetition rates could contribute to the development of new generations of particle injectors that may be suitable for medical proton therapy.

Journal Article↗

PubMed1993

Role of the glycosaminoglycan component of thrombomodulin in its acceleration of the inactivation of single-chain urokinase-type plasminogen activator by thrombin.

Thrombomodulin (TM), a membrane proteoglycan on endothelial cells, binds thrombin in a 1:1 complex, accelerates the protein C activation by thrombin, promotes the thrombin inactivation by antithrombin III and inhibits the procoagulant properties of thrombin. The inactivation of single-chain urokinase-type plasminogen activator (scu-PA) by thrombin is accelerated about 70-fold by TM [De Munk, Groeneveld and Rijken (1991) J. Clin. Invest. 88, 1680-1684]. The present study investigates the role of the O-linked glycosaminoglycan moiety of TM in the latter reaction. In the presence of an excess of a fully-glycosylated soluble recombinant human TM mutant (high-Mr rec-TM), 0.11 nM thrombin inactivated 50% of 4.4 nM scu-PA in 45 min at 37 degrees C. In the presence of a soluble recombinant TM mutant lacking the glycosaminoglycans (low-Mr rec-TM), 1.9 nM thrombin was needed to inactivate 50% scu-PA, as compared with 4.7 nM thrombin in the absence of TM. Using the scu-PA inactivation assay the dissociation constant for the thrombin-TM interaction was found to be 0.4 nM for high-Mr rec-TM and 14 nM for low-Mr rec-TM. Treatment of high-Mr rec-TM with chondroitinase ABC to digest the glycosaminoglycans decreased the accelerating effect to the level of low-Mr rec-TM. A similar decrease was observed after treatment of solubilized rabbit TM with chondroitinase ABC. As expected, chondroitinase ABC had no influence on the accelerating effect of low-Mr rec-TM. The free glycosaminoglycans obtained by alkaline treatment of TM or chondroitin sulphate A also accelerated the inactivation of scu-PA by thrombin, but about 1000-fold higher concentrations than with TM were needed to obtain the same acceleration. It is concluded that the major glycosaminoglycan of TM plays a pivotal role in the inactivation of scu-PA by the TM-thrombin complex, both in the formation and in the activity of the complex.

Chondroitin Lyases↗

PubMed1996

Memory lymphocytes from tuberculous effusions: purified protein derivative (PPD) stimulates accelerated activation marker expression and cell cycle progression.

Accelerated PPD-specific proliferation and generation of CD4+ cytotoxic effectors by mononuclear leucocytes (MNL) from tuberculous effusions (EMNL) has been previously reported by our laboratory. In order to explore the contribution of the state of activation of MNL to accelerated reactivity, EMNL and peripheral blood (PB)MNL from seven patients with tuberculosis were assessed both ex vivo and after PPD stimulation. Flow cytometry revealed no difference in the activation state (IL-2 receptor and HLA-DR expression) or cell cycle progression ex vivo. However, CD4+ CD29+ memory T cells were accumulated in EMNL compared with PBMNL. In vitro stimulation of EMNL with PPD resulted in accelerated expression of activation markers and progression through the cell cycle (peak after 4 days), whilst PBMNL exhibited normal activation kinetics (peak after 7 days). Accelerated reactivity could not be accounted for by quantitative differences in effusion CD4+ CD29+ memory T cells compared with blood, but may be due to a qualitative difference in effusion memory T cells, which are shown to be in a postactivation state of differentiation. T cells entering S and G2/M phases of the cell cycle were largely of the activated memory phenotype. Activation marker expression occurred in association with up-regulation of CD4 antigen expression on the surface of EMNL. Thus accelerated expression of activation markers and cell cycle progression by CD4+ CD29+ memory T cells may in part account for accelerated PPD reactivity in tuberculous effusions.

Adult↗

PubMed1996

Acceleration of IgE responses by treatment with recombinant interleukin-3 prior to infection with Trichinella spiralis in mice.

Treatment of mice with recombinant interleukin-3 (rIL-3) accelerated an IL-4-dependent IgE production following infection with Trichinella spiralis. When mice were treated with a total of 1.5 x 10(4) units rIL-3 for 5 days before infection with 400 muscle larvae, the serum IgE level increased prominently on day 5. Acceleration of IgE responses was dependent on the dose of rIL-3 injected. Treatment of mice with a total of 10(3) units rIL-3 could accelerate IgE responses. IgE responses were detected by a sandwich enzyme-linked immunosorbent assay at least from day 3 in mice treated with rIL-3. Acceleration of IgE responses was inhibited by anti-IL-4 monoclonal antibody. In contrast to this, IgG1 and IgG2a responses were not suppressed by the anti-IL-4 treatment. IL-3 treatment could up-regulate IgE and IgG1 responses but not the IgG2a response. IL-3 treatment could also accelerate IgE responses in W/Wv mice infected with the parasites. These results suggest that IL-3 is involved in regulation of IgE responses in mice and that mast cells do not play an essential role in acceleration of IgE responses induced by rIL-3 treatment in this system.

Animals↗

PubMed2003

Acceleration of Aux/IAA proteolysis is specific for auxin and independent of AXR1.

Aux/IAA proteins are short-lived transcriptional regulators involved in auxin signaling. Using Aux/IAA luciferase (LUC) fusion proteins expressed in Arabidopsis thaliana, we previously showed that rapid degradation of these proteins requires conserved Aux/IAA domain II and that exogenous auxin accelerates their degradation. To further examine auxin-mediated increases in proteolysis, the degradation of two other LUC fusion proteins, a non-cleavable ubiquitin LUC fusion (UB1-72::LUC) and SAUR15::LUC was determined in vivo in seedlings. Their half-lives were 20 +/- 4 and 104 +/- 10 min, respectively. SAUR15::LUC half-life was not affected by pre-incubation with 2,4-D. Auxin did not have an equivalent effect on UB(1-72)::LUC steady-state levels as compared to PsIAA6:LUC. LUC fused to an Aux/IAA domain II degraded more rapidly following auxin application, demonstrating that this region is sufficient for auxin-mediated acceleration of proteolysis. Hormonal cross-talk at the level of Aux/IAA proteolysis was examined. 1-aminocyclopropane-1-carboxylic acid (ACC), benzyladenine (BA), abscisic acid (ABA), and brassinolide (BL) did not affect the degradation rate of IAA1::LUC, and gibberellic acid (GA3) and salicylic acid (SA) did not specifically affect the steady-state levels of Aux/IAA::LUC proteins. An Aux/IAA::LUC transgene was crossed into the auxin resistant-1 (axr1-12) background. In axr1-12, the half-life of PsIAA6(1-73)::LUC increased 4.5-fold, but proteolysis still accelerated in response to exogenous auxin. These data suggest that auxin is the only phytohormone that accelerates Aux/IAA proteolysis, and that this acceleration is specific for Aux/IAA proteins. In addition, AXR1 plays an important role in rapid basal proteolysis of Aux/IAA proteins, but is not required for auxin-mediated acceleration of their degradation.

Amino Acids, Cyclic↗

PubMed1999

Acute toxicity and cost analysis of a phase III randomized trial of accelerated and conventional radiotherapy for squamous carcinoma of the head and neck: a Trans-Tasman Radiation Oncology Group study.

The primary purpose of the present analysis was to assess the feasibility and acute toxicity of a pure accelerated fractionation regimen in a cooperative group setting. This analysis included the first 320 patients entered on to the Trans-Tasman Radiation Oncology Group (TROG) randomized controlled trial which compared accelerated radiotherapy (ART) with conventional radiotherapy (CRT) in stage III and IV squamous cell carcinoma (SCC) of the head and neck. Patients were randomized to either 59.4 Gy in 33 fractions over 24 days (ART) or to 70 Gy 35 fractions over 49 days (CRT) after being stratified for site and stage. Accrual began in 1991 and the trial was closed on 3 April 1998 with the targeted 350 patients. The 3-year survival for the whole group was 54%, and the 3-year disease-free survival was 41%. Toxicity data were available on 303 patients (148 ART; 155 CRT). Mucosal toxicity was worse in the accelerated arm, and it peaked approximately 3 weeks earlier than the conventional arm. Skin toxicity was equivalent but occurred approximately 7 days earlier in the accelerated arm. Acute effects in both arms healed completely. Hospitalization was more common in the ART arm (71 vs 52 patients; P = 0.01) but the total bed days in hospital was not greatly different (1707 bed days for ART and 1607 bed days for CRT). Patients were more likely to require nasogastric (NG) feeding in the ART arm (49 vs 33 patients; P = 0.02). There were 1157 NG feeding days for ART and 1154 NG feeding days for CRT. The average cost of radiation treatment per patient including hospitalization, NG feeding and accommodation was $11,750 in the ART arm and $11,587 in the CRT arm. The accelerated arm has been shown to be a tolerable, practical and cost-equivalent regimen. The assessment of the therapeutic ratio of this accelerated protocol (ART) will be determined when the analysis of late effects and loco-regional control is made when the data are more mature.

Adult↗

PubMed2004

Concomitant radiochemotherapy or accelerated radiotherapy: analysis of two randomized trials of the French Head and Neck Cancer Group (GORTEC).

In the early 1990s, when conventional radiotherapy (RT) was the standard of care in patients with locally advanced head and neck squamous cell carcinoma (HNSCC), two main options were being tested to improve the efficacy and the therapeutic ratio of RT. The first approach evaluated the effect of adding chemotherapy (CT) simultaneously to RT (RT-CT), while the second approach assessed the effect of modified fractionated RT. To answer these two questions, in 1994, the French Group for Head and Neck Oncology Radiotherapy (GORTEC) initiated two randomized trials. A total of 494 patients were entered in these two parallel phase III multicenter trials comparing conventional RT (70 Gy in 35 fractions) either with concomitant RT-CT (226 patients; 70 Gy in 35 fractions with three cycles of a 4-day regimen comprising carboplatin and 5-fluorouracil [5FU]) or with very accelerated RT (268 patients) delivering 64 Gy in 3 weeks. The 5-year overall survival (OS), specific disease-free survival (DFS), and local-regional control rates were improved in favor of simultaneous RT-CT, whereas local-regional control was significantly improved with accelerated RT, along with a marginal effect on OS and DFS. This increased antitumor efficacy was in both cases associated with a marked increase in acute RT-induced toxicity, which was more pronounced with accelerated RT, whereas late effects were marginally increased with the addition of CT and not influenced by accelerated RT. We conclude that both concomitant RT-CT and accelerated RT improved tumor control rates, as compared to conventional RT, along with increased but manageable toxicity. The two regimens are currently being tested in an ongoing randomized study and also being compared to moderately accelerated RT and concomitant CT.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2003

Immunogenicity of an accelerated vaccination regime with a combined hepatitis a/b vaccine in patients with chronic hepatitis C.

OBJECTIVES: Hepatitis A (HAV) and B (HBV) vaccinations are recommended in patients with chronic liver diseases. METHODS: We prospectively investigated immunogenicity and safety of an accelerated vaccination protocol (0-7-21 days) with the combined hepatitis A/B vaccine (Twinrix(R)) versus the standard vaccination scheme (0-1-6 months) in hepatitis C virus-infected patients versus healthy volunteers. RESULTS: Local and general symptoms were mostly mild in all groups. One month after completion of the accelerated vaccination or standard vaccination, with the combined hepatitis A/B vaccine anti-HAV seroconversion rates (>33 IU/l) were 89 % and 88 % in HCV-infected patients. Initial HCV-nonresponders developed protective anti-HAV antibodies in 94 % and 96 % after a booster dose. According to the anti-HBs seroprotection rate, HCV-infected patients developed protective anti-HBs titres (>10 IU/l) in 77 % and 82 % of cases one month after the accelerated and the standard vaccination scheme-at month 2 and 7, respectively. This anti-HBs seroprotection rate could even be increased to 84 % and 85 % when initial HCV-infected nonresponders where given a booster dose with the combined hepatitis A/B vaccine. Protective anti-HAV and anti-HBs titers were achieved as early as month 2 after the accelerated vaccination schedule in the majority of HCV-infected patients. Healthy subjects developed protective anti-HAV titers and anti-HBs titers in 100 % and 98 % after the accelerated and standard vaccination protocol. CONCLUSIONS: This study is the first to have demonstrated that the accelerated combined hepatitis A/B vaccination is both safe and highly immunogenic against HAV and HBV in HCV-infected patients with well compensated liver disease.

Adolescent↗

PubMed2001

Accelerated internalization and detoxification of endotoxin by anti-lipopolysaccharide antibody is an Fc receptor--mediated process.

BACKGROUND: Interaction between lipopolysaccharide (LPS), LPS-binding protein, and the CD14 receptor at the surface of LPS-responsive cells results in inflammatory cytokine release and internalization and detoxification of LPS. Monoclonal antibodies (mAbs) raised against the deep-core lipid A or the O-linked polysaccharide moieties of LPS accelerate internalization and detoxification of LPS without stimulating cytokine release. This study was conducted to test the hypothesis that the antibody-mediated internalization of LPS is an Fc receptor (FcR)--mediated process. METHODS: Fluoroisothiocyanate (FITC)-conjugated Escherichia coli O111:B4 LPS was incubated with RAW 264.7 cells and allowed to internalize for 2 hours in the presence and absence of anti-LPS, anti-CD14, and isotype control mAbs, and Fab fragments from the anti-CD14, anti--Fc receptor, and control mAbs. Tumor necrosis factor--alpha (TNF-alpha) release was measured by WEHI 164 cell bioassay. FITC-LPS uptake was measured by flow cytometry. Statistical analysis was by analysis of variance and Fisher exact test. RESULTS: Addition of anti-LPS antibodies resulted in a 30- to 40-fold acceleration of LPS internalization (P <.01) in agreement with previous studies. This increase was blunted by anti-CD14 and also by isotype control holo-antibody (P <.01), but not by Fab fragments from anti-CD14 or isotype control antibody. Both anti-FcR antibodies and Fab fragments blocked anti-LPS antibody--stimulated uptake of FITC-LPS. Both intact anti-CD14 holo-antibody and Fab fragments blocked TNF-alpha release (P <.01). CONCLUSIONS: Clearance and detoxification of LPS are thought to be essential to the host response to endotoxin. It has been shown that antibodies to LPS accelerate its internalization by monocytic cell lines without increasing the elaboration of cytokines. We found that specific blockade of CD14 by Fab fragments could block TNF-alpha release but not alter the accelerated internalization of LPS produced by anti-LPS antibodies. In contrast, a nonspecific blockade of internalization was produced by competing antibody, which suggests a mechanistic role for the FcR. Specific blockade of FcR by either holo-antibody or Fab fragments blocked accelerated internalization, which confirms a FcR mechanism. We conclude that the accelerated internalization of LPS produced by anti-LPS antibody is an Fc receptor--mediated process. These results have significance for the development of adjuvant immunotherapy for gram-negative bacterial sepsis.

Animals↗

PubMed2003

A corresponding tyrosine residue in the C2/factor B type A domain is a hot spot in the decay acceleration of the complement C3 convertases.

The cleavage of C3 by the C3 convertases (C3bBb and C4b2a) determines whether complement activation proceeds. Dissociation (decay acceleration) of these central enzymes by the regulators decay-accelerating factor (DAF), complement receptor 1 (CR1), factor H, and C4-binding protein (C4BP) controls their function. In a previous investigation, we obtained evidence implicating the alpha4/5 region of the type A domain of Bb (especially Tyr338) in decay acceleration of C3bBb and proposed this site as a potential interaction point with DAF and long homologous repeat A of CR1. Because portions of only two DAF complement control protein domains (CCPs), CCP2 and CCP3, are necessary to mediate its decay of the CP C3 convertase (as opposed to portions of at least three CCPs in all other cases, e.g. CCPs 1-3 of CR1), DAF/C4b2a provides the simplest structural model for this reaction. Therefore, we examined the importance of the C2 alpha4/5 site on decay acceleration of C4b2a. Functional C4b2a complexes made with the C2 Y327A mutant, the C2 homolog to factor B Y338A, were highly resistant to DAF, C4BP, and long homologous repeat A of CR1, whereas C2 substitutions in two nearby residues (N324A and L328A) resulted in partial resistance. Our new findings indicate that the alpha4/5 region of C2a is critical to decay acceleration mediated by DAF, C4BP, and CR1 and suggest that decay acceleration of C4b2a and C3bBb requires interaction of the convertase alpha4/5 region with a CCP2/CCP3 site of DAF or structurally homologous sites of CR1 and C4BP.

Amino Acid Sequence↗

PubMed2001

The vestibular evoked response to linear, alternating, acceleration pulses without acoustic masking as a parameter of vestibular function.

In this study, short latency vestibular evoked potentials (VsEPs) were recorded in five guinea pigs in response to alternating linear acceleration pulses with and without acoustic masking. A steel bolt was implanted in the skull and coupled to a shaker. Linear acceleration pulses (n = 400) in upward, downward or alternating directions were given, with a peak acceleration of 4g after 0.5 msec. Tests were repeated with acoustic masking, after modiolus destruction and after application of KCl in the vestibule. Stimuli of the vestibular nerve were recorded with a platinum electrode in the bony facial nerve canal in the bulla. Unilateral linear acceleration showed a shallow plateau at 0.5 msec, which disappeared with alternating acceleration impulses and after modiolus destruction. Therefore all further tests were done with alternating impulses. After a latency time of 0.8 msec a multiwave response was seen, with a first positive peak P1 at 1.16 ms. These were followed by other positive and negative peaks (N1, P2, N2, P3, N3). With the elimination of cochlear influences by using acoustic masking, P1 remained stable, while subsequent peaks were altered or eliminated. After modiolus destruction, the P1 peak remained, although with a smaller amplitude due to vestibular damage. After application of a saturated KCl solution in the vestibule all responses, including P1, disappeared, thus confirming the vestibular origin of these responses. We conclude that the onset latency of the VsEP and the peak latency and level of the first positive peak P1 in response to alternating linear acceleration pulses without acoustic masking, measured in the facial canal, are good and stable parameters of vestibular function in guinea pigs.

Animals↗

PubMed2006

Evaluation of accelerated iterative x-ray CT image reconstruction using floating point graphics hardware.

Statistical reconstruction methods offer possibilities to improve image quality as compared with analytical methods, but current reconstruction times prohibit routine application in clinical and micro-CT. In particular, for cone-beam x-ray CT, the use of graphics hardware has been proposed to accelerate the forward and back-projection operations, in order to reduce reconstruction times. In the past, wide application of this texture hardware mapping approach was hampered owing to limited intrinsic accuracy. Recently, however, floating point precision has become available in the latest generation commodity graphics cards. In this paper, we utilize this feature to construct a graphics hardware accelerated version of the ordered subset convex reconstruction algorithm. The aims of this paper are (i) to study the impact of using graphics hardware acceleration for statistical reconstruction on the reconstructed image accuracy and (ii) to measure the speed increase one can obtain by using graphics hardware acceleration. We compare the unaccelerated algorithm with the graphics hardware accelerated version, and for the latter we consider two different interpolation techniques. A simulation study of a micro-CT scanner with a mathematical phantom shows that at almost preserved reconstructed image accuracy, speed-ups of a factor 40 to 222 can be achieved, compared with the unaccelerated algorithm, and depending on the phantom and detector sizes. Reconstruction from physical phantom data reconfirms the usability of the accelerated algorithm for practical cases.

Algorithms↗

PubMed1993

Accelerated hypertension--patterns of mortality and clinical factors affecting outcome in treated patients.

We evaluated the outcome of patients presenting with accelerated hypertension, as part of an audit of the Aberdeen Hypertension Clinic database. Of 3928 patients (2005 male, 1923 female) referred for assessment of hypertension, 128 (77 male, 51 female) presented with accelerated hypertension. The main outcome measures were systolic and diastolic pressure, length of time from referral to death or censor date, and cause of death. Accelerated hypertensives had a higher death rate than other hypertensives. Using life-table analysis, age and serum creatinine at referral were sufficient to predict survival. Almost 50% (15/31) of the deceased accelerated hypertensives died of acute myocardial infarction. Mean survival after referral was estimated as 18 years for accelerated hypertensives (mean referral age 52 years) and 21 years for other hypertensives (mean referral age 48 years). Blood pressure fell most during the first year of treatment, and declined steadily thereafter. Systolic blood pressure fell by a mean of 50 mmHg and diastolic pressure by 30 mmHg in the first year, and at about 2 (diastolic) and 1 (systolic) mmHg/year for the next 10 years. Thus although the prognosis for accelerated hypertensives is not quite as good as for other hypertensives, with suitable care they can survive for a considerable period.

Adult↗

PubMed1998

Exposure of vascular allografts to insulin-like growth factor-I (IGF-I) increases vascular expression of IGF-I ligand and receptor protein and accelerates arteriosclerosis in rats.

BACKGROUND: Accelerated arteriosclerosis limits the survival of transplanted hearts. We hypothesized that insulin-like growth factor-I (IGF-I) is crucial in accelerating transplant arteriosclerosis. Recently, we reported that exposure to IGF-I prior to transplantation accelerates transplant arteriosclerosis in the rat aorta allograft model. Here, we studied the mechanism whereby IGF-I exposure accelerates transplant arteriosclerosis. METHODS: The abdominal aorta was harvested from male Brown Norway rats and exposed to 0, 200, or 500 ng/ml of IGF-I at 37 degrees C for 30 min prior to transplantation to the abdominal position of male Lewis rats. The allografts were harvested 14 days later and processed for immunohistochemical staining for alpha-actin, growth factors (IGF-I, IGF-I receptor, platelet-derived growth factor-BB, and basic fibroblast growth factor), and immunological markers (major histocompatibility complex class II antigen, macrophage, and CD4- and CD8-positive T cells). RESULTS: By 14 days, the ex vivo IGF-I donor aorta treatment with IGF-I increased in a concentration-dependent manner the expression of IGF-I and IGF-I receptor in both the intima and the adventitia. In contrast, the expression of platelet-derived growth factor-BB was decreased in a concentration-dependent manner in the intima while basic fibroblast growth factor remained unchanged. The cell-mediated immune response was not affected by IGF-I at 14 days after transplantation, which suggests that the immune events associated with acceleration of transplant arteriosclerosis may occur at an earlier time. CONCLUSION: Acceleration of transplant arteriosclerosis by exposure to IGF-I is associated with increased IGF-I ligand and receptor expression in the allograft vascular wall. These data further suggest that IGF-I may be a major factor in mediating graft arteriosclerosis.

Actins↗

PubMed2002

Acceleration effect of coupled oscillator systems.

We have developed a curved isochron clock (CIC) by modifying the radial isochron clock to provide a clean example of the acceleration (deceleration) effect. By analyzing a two-body system of coupled CICs, we determined that an unbalanced mutual interaction caused by curved isochron sets is the minimum mechanism needed for generating the acceleration (deceleration) effect in coupled oscillator systems. From this we can see that the Sakaguchi and Kuramoto (SK) model, which is a class of nonfrustrated mean field model, has an acceleration (deceleration) effect mechanism. To study frustrated coupled oscillator systems, we extended the SK model to two oscillator associative memory models, one with symmetric and the other with asymmetric dilution of coupling, which also have the minimum mechanism of the acceleration (deceleration) effect. We theoretically found that the Onsager reaction term (ORT), which is unique to frustrated systems, plays an important role in the acceleration (deceleration) effect. These two models are ideal for evaluating the effect of the ORT because, with the exception of the ORT, they have the same order parameter equations. We found that the two models have identical macroscopic properties, except for the acceleration effect caused by the ORT. By comparing the results of the two models, we can extract the effect of the ORT from only the rotation speeds of the oscillators.

Animals↗

PubMed2003

Onset of turbulence in accelerated high-Reynolds-number flow.

A new criterion, flow drive time, is identified here as a necessary condition for transition to turbulence in accelerated, unsteady flows. Compressible, high-Reynolds-number flows initiated, for example, in shock tubes, supersonic wind tunnels with practical limitations on dimensions or reservoir capacity, and high energy density pulsed laser target vaporization experimental facilities may not provide flow duration adequate for turbulence development. In addition, for critical periods of the overall flow development, the driving background flow is often unsteady in the experiments as well as in the physical flow situations they are designed to mimic. In these situations transition to fully developed turbulence may not be realized despite achievement of flow Reynolds numbers associated with or exceeding stationary flow transitional criteria. Basically our transitional criterion and prediction procedure extends to accelerated, unsteady background flow situations the remarkably universal mixing transition criterion proposed by Dimotakis [P. E. Dimotakis, J. Fluid Mech. 409, 69 (2000)] for stationary flows. This provides a basis for the requisite space and time scaling. The emphasis here is placed on variable density flow instabilities initiated by constant acceleration Rayleigh-Taylor instability (RTI) or impulsive (shock) acceleration Richtmyer-Meshkov instability (RMI) or combinations of both. The significant influences of compressibility on these developing transitional flows are discussed with their implications on the procedural model development. A fresh perspective for predictive modeling and design of experiments for the instability growth and turbulent mixing transitional interval is provided using an analogy between the well-established buoyancy-drag model with applications of a hierarchy of single point turbulent transport closure models. Experimental comparisons with the procedural results are presented where use is made of three distinctly different types of acceleration driven instability experiments: (1) classical, relatively low speed, constant acceleration RTI experiments; (2) shock tube, shockwave driven RMI flow mixing experiments; (3) laser target vaporization RTI and RMI mixing experiments driven at very high energy density. These last named experiments are of special interest as they provide scaleable flow conditions simulating those of astrophysical magnitude such as shock-driven hydrodynamic mixing in supernova evolution research.

Journal Article↗

PubMed2005

Intermittency of acceleration in isotropic turbulence.

The intermittency of acceleration is investigated for isotropic turbulence using direct numerical simulation. Intermittently found acceleration of large magnitude always points towards the rotational axis of a vortex filament, indicating that the intermittency of acceleration is associated with the rotational motion of the vortices that causes centripetal acceleration, which is consistent with the reported result for the near-wall turbulence. Furthermore, investigation on movements of such vortex filaments provides some insights into the dynamics of local dissipation, enstrophy and acceleration. Strong dissipation partially covering the edge of a vortex filament shows weak correlation with enstrophy, while it is strongly correlated with acceleration.

Journal Article↗