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PubMed2004

Smoking accelerates biotin catabolism in women.

BACKGROUND: Smoking accelerates the degradation of many nutrients, including lipids, antioxidants, and certain B vitamins. Accelerated biotin catabolism is of concern in women because marginal biotin deficiency is teratogenic in mammals. OBJECTIVE: The objective was to assess the effect of smoking on the biotin status of women. DESIGN: A preliminary study of 7 women and 3 men examined the urinary concentrations of biotin and its metabolites biotin sulfoxide and bisnorbiotin in smokers. The interpretation of the results of this study was limited by the lack of a contemporaneous control group; consequently, we conducted a cohort-controlled study. Smoking women (n = 8) and nonsmoking control subjects (n = 15) provided 24-h urine samples; excretion rates of biotin, the biotin metabolites, and 3-hydroxyisovaleric acid were determined. Increased urinary excretion of 3-hydroxyisovaleric acid, which reflects a reduced activity of the biotin-dependent enzyme 3-methylcrotonyl-Co A carboxylase, is a sensitive indicator of biotin depletion at the tissue level. RESULTS: Compared with control subjects from previous studies, the smoking women in the preliminary study excreted significantly less urinary biotin (P = 0.02). Moreover, the ratio of urinary biotin sulfoxide to biotin increased (P = 0.04) in these women. In the cohort-controlled study, the urinary excretion of biotin decreased by 30% (P = 0.04), and the ratios of urinary bisnorbiotin and biotin sulfoxide to biotin increased significantly, which indicated accelerated catabolism in smokers. Moreover, the urinary excretion of 3-hydroxyisovaleric acid was greater in the smokers than in the control subjects (P = 0.04), which indicated biotin depletion in the smokers at the tissue level. CONCLUSION: These data provide evidence of accelerated biotin metabolism in smoking women, which results in marginal biotin deficiency.

Adult↗

PubMed1997

Postmenopausal acceleration of age-related mortality increase.

The force of natural selection to eliminate deleterious genes is attenuated with advancing age, allowing senescence to evolve. This suggests that a distinctly marked end of the reproduction period is likely to be followed by an acceleration of senescence. It is thus expected that menopause should trigger an acceleration of age-related mortality increase in human females. Such an abrupt initiation of mortality acceleration is not predicted for human males at the same ages, whose fecundity declines more gradually. Life table aging rate patterns for selected industrialized countries generally support this hypothesis. A cause-of-death decomposition analysis indicates that the sex differential in mortality acceleration is mainly due to cardiovascular diseases, which is consistent with the prevalent view that postmenopausal changes in the sex hormone status may affect lipoprotein metabolism, and in turn, raise the risk of arteriosclerosis.

Adult↗

PubMed1999

Aminoguanidine supplementation delays the onset of senescence in vitro in dermal fibroblast-like cells from senescence-accelerated mice.

The effects of aminoguanidine supplementation on senescence acceleration in vitro were examined in fibroblasts from the dorsal dermis of newborn SAMP11 (accelerated senescence-prone mice), and were compared to the effects in cell lines from SAMR1 (accelerated senescence-resistant) mice. Four millimolar aminoguanidine supplementation significantly delayed the senescence/crisis in cell lines from SAMP11 mice, but did not affect the senescence/crisis in cell lines from SAMR1 mice. Flow cytometric analysis of the DNA content of confluent cells revealed that aminoguanidine supplementation significantly decelerated the increase in the number of tetraploid cells until senescence/crisis. Although mean concentrations of lipid peroxides in the primary cultures did not differ significantly, considerably higher lipid peroxidation was observed in some SAMP11 cultures, and aminoguanidine supplementation reduced them to the levels in SAMRI cultures. These results strongly suggest that oxidative stress derived from polyamine catabolism may contribute to the senescence acceleration in vitro in cell lines from SAMP11 mice.

Animals↗

PubMed2005

Cultured murine dermal fibroblast-like cells from senescence-accelerated mice as in vitro models for higher oxidative stress due to mitochondrial alterations.

The senescence-accelerated mouse is a model for senescence acceleration, a higher oxidative stress status, and age-associated disorders. We studied whether fibroblasts cultured from accelerated senescence-prone SAMP11 mice could be used as in vitro models for oxidative stress in senescence. Dichlorofluorescein and hydroethidine assays demonstrated that cells from SAMP11 mice produced more reactive oxygen species than did cells from accelerated senescence-resistant SAMR1 mice. These differences were not due to the defective induction of antioxidants. Double labeling with hydroethidine and MitoTracker Green revealed that most of the reactive oxygen species were generated within the mitochondria. Nonyl acridine orange and JC-1 assays showed an increase in the mass of the mitochondria, especially those with low membrane potential, in SAMP11 cells. Ultrastructurally, mitochondria with degenerative morphology were increased in SAMP11 cells with longer culture periods. These results suggest that cells from SAMP11 mice are useful models for spontaneous higher oxidative stress in vitro due to dysfunctional mitochondria.

Animals↗

PubMed2006

PGC-1beta down-regulation is associated with reduced ERRalpha activity and MCAD expression in skeletal muscle of senescence-accelerated mice.

Mitochondrial dysfunction is involved in the development of aging. Here, we examined the effect of aging on the skeletal muscle expression of two isoforms of the transcriptional peroxisome proliferator-activated receptor gamma (PPARgamma) coactivator-1 (PGC-1) in an experimental murine model of accelerated aging, the senescence-accelerated mouse (SAM). The senescence-accelerated prone mice (SAM-P8) showed no changes in PGC-1alpha, but a decrease in PGC-1beta expression (52% reduction, p <.001) was observed compared to the senescence-accelerated resistant mice (SAM-R1). In agreement with the proposed role of PGC-1beta as an estrogen-related receptor (ERR) protein ligand, the expression of the ERRalpha target gene medium-chain acyl-coenzyme A dehydrogenase was strongly suppressed (85%, p <.001) in SAM-P8. The decrease in the expression of medium-chain acyl-coenzyme A dehydrogenase was consistent with the reduction in ERRalpha DNA-binding activity of SAM-P8. These findings indicate that the age-mediated decrease in PGC-1beta expression in SAM-P8 skeletal muscle affects the expression of genes involved in mitochondrial fatty acid oxidation.

Acyl-CoA Dehydrogenase↗

PubMed2002

Acceleration of DNA strand exchange reaction by cationic polymers.

In previous reports, we have demonstrated that the cationic comb-type copolymers (PLL-g-Dex) having a poly-L-lysine main chain and dextran side chains stabilized DNA duplex and triplex. Furthermore, the copolymer was found to accelerate more than 20,000 folds strand exchange reaction between 20 bp duplex and its homologous single strand (1). This study was designed to inspect structural factor of polycationic moieties in acceleration effects. To this end, polypeptides containing lysine or arginine moieties as cationic groups were examined in their potency to accelerating strand exchange reaction. It was shown that arginine-rich peptide showed higher accelerating effect than lysine peptide when total positive charges of peptides were kept constant.

Amino Acid Sequence↗

PubMed1987

Accelerating effect of zinc ions on the surface-mediated activation of factor XII and prekallikrein.

The effect of zinc ions on the surface-mediated activation of factor XII and prekallikrein was studied, using the contact system reconstituted with the purified proteins from bovine and human plasmas. The sulfatide-mediated activation of factor XII and prekallikrein in the presence of high-molecular-weight (HMW) kininogen was remarkably accelerated by 10(-5) M zinc ions. This accelerating effect was observed only in the presence of HMW kininogen. The kinetic analysis of the accelerating effect of zinc ions demonstrated that zinc ions reduce the Km values and increase the Vmax values on the activation of factor XII by kallikrein and on the activation of prekallikrein by factor XIIa. The value of Vmax/Km increased 26.4-fold in the former reaction and 2.8-fold in the latter reaction, indicating that zinc ions accelerate mainly the activation of factor XII by kallikrein. In the presence of 5 x 10(-4) M zinc ions, typical difference spectra due to a red shift of tryptophan and/or tyrosine residues were observed for HMW kininogen and its derivatives but not low-molecular-weight (LMW) kininogen. Since the concentration of zinc ions required to induce the difference spectra is comparable with that to enhance the activation of factor XII and prekallikrein, it appears that there is some correlation between the conformational change of HMW kininogen and the enhancement of the activation.

Animals↗

PubMed1996

A progress report on accelerated residency programs in family practice.

BACKGROUND: In 1991 the American Board of Family Practice (ABFP) approved 12 programs to participate in an experiment in medical education. Selected students in 12 medical schools are able to complete their first year of family practice residency while completing their fourth year of school. This paper reports on the progress of the programs and residents participating in this project. METHOD: Data from the ABFP in-training examination and certification examination were compiled for all trainees and graduates through 1994. Performances were compared with national norms and the performances of traditional residents in the same programs. The program directors were surveyed to assess their experiences, program effectiveness, benefits, liabilities, and implementation problems. RESULTS: Accelerated residents performed better than their peers and national norms on the ABFP in-training and certification examinations. The directors rated the clinical performance of accelerated residents as equal to or better than the clinical performance of traditional residents by the end of the program. Advantages of accelerated residency included improvements in recruiting, image, and morale. Problems occurred in order and prescription writing and acceptance of the accelerated residents by nurses, other residents, and physicians in other disciplines. CONCLUSION: Early entry into residency training of bright, highly motivated, and mature students appears to offer benefits for trainees and programs alike.

Educational Measurement↗

PubMed1998

Gait biomechanics are not normal after anterior cruciate ligament reconstruction and accelerated rehabilitation.

PURPOSE: Accelerated rehabilitation for anterior cruciate ligament (ACL) injury and reconstruction surgery is designed to return injured people to athletic activities in approximately 6 months. The small amount of empirical data on this population suggests, however, that the torque at the knee joint may not return until 22 months after surgery during walking and even longer during running. Although the rehabilitation has ended and individuals have returned to preinjury activities, gait mechanics appear to be abnormal at the end of accelerated programs. The purpose of this study was to compare lower extremity joint kinematics, kinetics, and energetics between individuals having undergone ACL reconstruction and accelerated rehabilitation and healthy individuals. METHODS: Eight ACL-injured and 22 healthy subjects were tested. Injured subjects were tested 3 wk and 6 months (the end of rehabilitation) after surgery. Ground reaction force and kinematic data were combined with inverse dynamics to predict sagittal plane joint torques and powers from which angular impulse and work were derived. RESULTS: The difference in all kinematic variables between the two tests for the ACL group averaged 38% (all P < 0.05). The kinematics were not different between the ACL group after rehabilitation and healthy subjects. Angular impulses and work averaged 100% difference for all joints (all P < 0.05) between tests for the ACL group. After rehabilitation, the differences between injured and healthy groups in angular impulse and work at both the hip and knee remained large and averaged 52% (all P < 0.05). CONCLUSIONS: Results indicated that after reconstruction surgery and accelerated rehabilitation for ACL injury, humans walk with normal kinematic patterns but continue to use altered joint torque and power patterns.

Adult↗

PubMed1993

Reversal of ongoing heart, kidney, and pancreas allograft rejection and suppression of accelerated heart allograft rejection in the rat by rapamycin.

Rapamycin was examined for its effects on reversal of ongoing rejection of heart, kidney, and pancreas allografts and on suppression of accelerated heart allograft rejection in the rat. A 14-day continuous intravenous infusion of RAPA by an osmotic pump at 0.02, 0.08, and 0.8 mg/kg/day to WFu recipients, starting 4 days postoperation, significantly protected the BUF heart allografts with a mean survival time (MST) +/- 1 SD of 33.2 +/- 19.8 (p < 0.001), 48.2 +/- 14.8 (p < 0.001), and 107.0 +/- 86.3 (p < 0.001) days, respectively, as compared with 7.2 +/- 0.8 days in vehicle-treated controls. Combination of low dose RAPA (0.02 mg/kg or 0.08 mg/kg) and low dose CsA (2 mg/kg) achieved significantly longer cardiac allograft survival than RAPA or CsA alone. RAPA's effect in reversing ongoing rejection of renal and pancreatic allografts was also significant. The BUF kidney and pancreas in WFu recipients treated with a 14-day course of RAPA (0.8 mg/kg/day starting 4 days postoperation) had an MST of 44.7 +/- 15.9 (p < 0.001) and 46.4 +/- 12.5 (p < 0.001), while in vehicle-treated controls, the grafts were rejected within 10 days. RAPA could also suppress accelerated cardiac allograft rejection. Hyperimmunized WFu recipients were treated with two 14-day courses of continuous i.v. RAPA at 0.8 mg/kg/day before and after BUF heart allografting. Significantly longer survival of the grafts (25.5 +/- 3.7 days, p < 0.001) was achieved compared with that of the vehicle-treated controls (3.8 +/- 1.0 days). One-course RAPA treatment before or after heart transplantation was considerably less effective. RAPA was also shown to prevent the increase of serum IgG levels and to inhibit the production of specific cytotoxic Ab in the rat receiving repetitive immunizations. Such effects presumably contribute to the inhibition of the accelerated rejection. The results of this study suggest that RAPA is potentially useful in treatment of ongoing as well as accelerated allograft rejection.

Animals↗

PubMed1994

Regeneration-induced accelerated rejection in reduced-size liver grafts.

Liver regenerative processes are associated with enhanced expression of alloantigens. Accordingly, we tested the hypothesis that such enhanced surface expression of alloantigens during regeneration of reduced-size liver grafts is associated with accelerated rejection. Our OLT model was LEW (RT1) to BN (RT1n), with donor liver resected by 50%. The study group consisted of reduced-size allografts. Control groups were syngeneic reduced-size isografts and full-size allografts. Reduced-size isograft recipients survived indefinitely. Both isografts and allografts regenerated to their prereduction size within 12 days. Recipients of reduced-size allografts died of accelerated rejection within 12.2 +/- 0.8 days, significantly earlier than recipients receiving full-size allografts (36.2 +/- 4.1 days, P < 0.01). The accelerated rejection in the regenerating allografts was mediated both by cellular and humoral mechanisms, evidenced by earlier lymphocytic invasion of the graft, enhanced donor MHC class II expression, and the emergence of IgM antibodies, directed specifically against donor endothelial antigens. These data suggest that regeneration of reduced-size allografts is accompanied by accelerated cellularly and humorally mediated alloreactivity. Recipients of reduced-size allografts may, therefore, benefit from more potent immunosuppression during the period of active liver regeneration.

Animals↗

PubMed1998

Importance of T cells to accelerated rejection and acceptance of renal allografts in sensitized rat recipients.

BACKGROUND: Sensitized recipients often experience fulminant allograft loss by yet ill-defined cellular and/or humoral immune mechanisms. In this study, we analyzed the contribution of cellular elements, in particular T cells, to the accelerated rejection of renal allografts in sensitized rats. METHODS AND RESULTS: LEW rats sensitized with BN skin grafts died of uremia in 3.3+/-0.9 days after transplantation of a BN kidney, similarly to bilaterally nephrectomized animals. Adoptive transfer of 10(6) graft-infiltrating mononuclear cells as well as their CD25+ subset into otherwise normal LEW recipients accelerated rejection of BN test cardiac allografts (5.4+/-0.5 days to 6.6+/-0.4 days vs. 7.8+/-0.8 days in controls, P<0.0007), while the CD25- population was ineffective (8.0+/-0.6 days, NS). Furthermore, alpha/beta-T-cell receptor (TCR)-targeted therapy with R73 monoclonal antibody abrogated accelerated rejection, and produced long-term survival in sensitized animals treated before kidney engraftment (day -7 to day -1). Long-term survival was associated with an up-regulation of intragraft interleukin-4 and interleukin-10 expression in conjunction with depressed Th-1-type cytokines. In addition, alpha/beta-TCR-targeted therapy even in low subtherapeutic dose decreased IgM alloantibody levels, and prevented the switch from IgM to IgG alloantibody response. CONCLUSIONS: This is the first report that documents the striking efficacy of alpha/beta-TCR-targeted therapy in sensitized rat renal transplant recipients. The results provide evidence for a critical role of T cells for both accelerated rejection and long-term graft survival. Up-regulation of Th2-type cytokine profile may, at least in part, contribute to the acquisition of immune unresponsiveness after alpha/beta-TCR-targeted therapy in this well-defined rat renal transplant model.

Adoptive Transfer↗

PubMed2001

Immunogenicity of two accelerated hepatitis B vaccination protocols in liver transplant candidates.

OBJECTIVE: It is common practice to immunize patients against hepatitis B virus infection prior to orthotopic liver transplantation (OLT). We compared the seroprotection rates of two accelerated schedules with a recombinant hepatitis B vaccine in patients awaiting OLT. DESIGN AND METHODS: Patients were prospectively recruited and vaccinated with either 20 micrograms (group 1, n = 14) or 40 micrograms (group 2, n = 20) hepatitis B surface antigen per dosage. Thirty-nine healthy volunteers served as a historical control group. Patients in all groups were vaccinated with an accelerated schedule (0, 7 and 21 days). All patients underwent clinical and laboratory examinations (HBs antibodies, CD4/CD8 ratio, transaminases). RESULTS: The accelerated hepatitis B vaccination schedules were well tolerated. Eight weeks after the third injection, no significant differences in seroprotection rates were observed between group 1 (31%) and group 2 (26%). There was no correlation with respect to seroconversion rates and gender, smoking habits or CD4/CD8 ratio. CONCLUSION: These data suggest that accelerated vaccination schedules with a recombinant hepatitis B vaccine are safe and well-tolerated, but only achieve poor seroconversion rates in OLT candidates. Increasing the vaccine dose to 40 micrograms hepatitis B surface antigen per injection did not result in a higher response rate. Because of the low risk of acquiring de novo hepatitis B infection after transplantation, it should be questioned whether routine hepatitis B vaccination with standard recombinant vaccines prior to liver transplantation should be recommended any longer.

Adult↗

PubMed2006

Estrogen replacement effectively improves the accelerated intimal hyperplasia following balloon injury of carotid artery in the ovariectomized rats.

Present experiments were designed to investigate the effects of ovariectomy (OVX) and estrogen replacement (ER) on neointimal formation after balloon injury of the rat carotid artery. Young adult female rats were divided into 3 groups of sham operation (control), ovariectomy, and ovariectomy plus estrogen replacement. Estrogen replacement was initiated by implanting a sustained release pellet containing water-soluble 17beta-estradiol 1 week after the ovariectomy. Carotid arteries were harvested 2 weeks after the balloon injury for determinations. The balloon injury caused intimal hyperplasia, which was accompanied by the impaired endothelium-dependent relaxation and cyclic GMP production, and accumulation of asymmetric dimethylarginine (ADMA) as an endogenous NOS inhibitor. Bilateral ovariectomy accelerated the intimal hyperplasia. The acceleration was accompanied by the enhanced impairment of NO production, attenuated reendothelialization, and enhanced accumulation of ADMA. The estrogen replacement improved the accelerated intimal hyperplasia with concomitant improvement of the impaired NO production and accumulated asymmetric dimethylarginine, and facilitated reendothelialization. These results suggests that the enhanced impairment of NO production, which possibly results from the accumulated asymmetric dimethylarginine and lack of reendothelialization, may contribute to the acceleration of intimal hyperplasia by ovariectomy and that estrogen replacement effectively improves the intimal hyperplasia by restoring the impaired NO production through reducing endogenous NOS inhibitor and facilitating reendothelialization.

Animals↗

PubMed2006

Three-dimensional cerebral contrast-enhanced magnetic resonance venography at 3.0 Tesla: initial results using highly accelerated parallel acquisition.

OBJECTIVE: The objective of this study was to evaluate a high spatial resolution 3-dimensional (3D) contrast-enhanced magnetic resonance (CE-MR) venography protocol for evaluation of intracranial venous system using highly accelerated parallel imaging at 3.0 T. MATERIALS AND METHODS: Ten patients (4 male, 6 female; age, 38-76 years) with suspected cerebrovascular disease were prospectively studied on a 32-channel 3.0 T MR system. After a single intravenous contrast injection, high spatial resolution 3D CE-MR angiography of the entire supraaortic arteries was performed followed immediately by 3D cerebral CE-MR venography. By using a fast 3D gradient-recalled-echo sequence with elliptic centric k-space ordering and highly accelerated parallel acquisition (acceleration factor 3 and 2 in phase and slice encoding direction, respectively), 3D cerebral CE-MR venography was acquired with voxel dimensions of 0.7 x 0.7 x 0.8 mm in 24 seconds. Image evaluation was performed independently by 2 neuroradiologists for overall image quality, presence of noise, and artifacts. The image quality of 30 venous segments was evaluated in each subject using a 1 to 4 scoring scale. In 2 patients, catheter angiography was available for correlation. Statistical analysis of data was performed by using Wilcoxon rank sum test and kappa coefficient. RESULTS: All studies were determined to be of diagnostic image quality by both observers. The majority (90%) of cerebral venous segments were evaluated to be of diagnostic image quality (median, 3; range, 3-4) by both readers and with excellent interobserver agreement (kappa = 0.86; 95% confidence interval, 0.79-0.93). One meningioma invading the superior sagittal sinus and one superior sagittal sinus fistula were detected subsequently confirmed by conventional angiography. CONCLUSION: High spatial resolution 3D cerebral CE-MR venography is feasible and promising. Using a 32-channel 3.0 T system combined with multichannel array coils effectively supports highly accelerated parallel imaging, enabling subsequent acquisition of both high spatial resolution CE-MR angiography and CE-MR venography after a single contrast injection without impairing the image quality. More extensive clinical studies are warranted to establish the range of applications and confirm the accuracy of this technique.

Adult↗

PubMed2006

Laser-plasma accelerator: status and perspectives.

Laser-plasma accelerators deliver high-charge quasi-monoenergetic electron beams with properties of interest for many applications. Their angular divergence, limited to a few mrad, permits one to generate a small gamma ray source for dense matter radiography, whereas their duration (few tens of fs) permits studies of major importance in the context of fast chemistry for example. In addition, injecting these electron beams into a longer plasma wave structure will extend their energy to the GeV range. A GeV laser-based accelerator scheme is presented; it consists of the acceleration of this electron beam into relativistic plasma waves driven by a laser. This compact approach (centimetres scale for the plasma, and tens of meters for the whole facility) will allow a miniaturization and cost reduction of future accelerators and derived X-ray free electron laser (XFEL) sources.

Journal Article↗

PubMed2006

Laser wakefield acceleration: the injection issue. Overview and latest results.

External injection of electron bunches into laser-driven plasma waves so far has not resulted in 'controlled' acceleration, i.e. production of bunches with well-defined energy spread. Recent simulations, however, predict that narrow distributions can be achieved, provided the conditions for properly trapping the injected electrons are met. Under these conditions, injected bunch lengths of one to several plasma wavelengths are acceptable. This paper first describes current efforts to demonstrate this experimentally, using state-of-the-art radio frequency technology. The expected charge accelerated, however, is still low for most applications. In the second part, the paper addresses a number of novel concepts for significant enhancement of photo-injector brightness. Simulations predict that, once these concepts are realized, external injection into a wakefield accelerator will lead to accelerated bunch specs comparable to those of recent 'laser-into-gasjet' experiments, without the present irreproducibility of charge and final energy of the latter.

Journal Article↗

PubMed2006

High-intensity laser-driven proton acceleration: influence of pulse contrast.

Proton acceleration from the interaction of ultra-short laser pulses with thin foil targets at intensities greater than 10(18) W cm(-2) is discussed. An overview of the physical processes giving rise to the generation of protons with multi-MeV energies, in well defined beams with excellent spatial quality, is presented. Specifically, the discussion centres on the influence of laser pulse contrast on the spatial and energy distributions of accelerated proton beams. Results from an ongoing experimental investigation of proton acceleration using the 10 Hz multi-terawatt Ti:sapphire laser (35f s, 35 TW) at the Lund Laser Centre are discussed. It is demonstrated that a window of amplified spontaneous emission (ASE) conditions exist, for which the direction of proton emission is sensitive to the ASE-pedestal preceding the peak of the laser pulse, and that by significantly improving the temporal contrast, using plasma mirrors, efficient proton acceleration is observed from target foils with thickness less than 50 nm.

Journal Article↗