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PubMed2002

Comparison between continuous accelerated hyperfractionated and late-course accelerated hyperfractionated radiotherapy for esophageal carcinoma.

PURPOSE: To compare the treatment results and toxicity of continuous accelerated hyperfractionated (CAHF) and late-course accelerated hyperfractionated (LCAF) radiotherapy (RT) for esophageal carcinoma. METHODS AND MATERIALS: Between August 1996 and March 1999, 101 patients with squamous cell carcinoma of the esophagus were randomized into two groups: 49 to the CAHF group and 52 to the LCAF group. Patients in the CAHF group received RT at 1.5 Gy/fraction b.i.d. (6-h interval), 5 d/wk, to a total dose 66 Gy in 44 fractions during 4.4 weeks. The patients in the LCAF group received conventional fractionation RT, 1.8 Gy/fraction, to a dose of 41.4 Gy in 23 fractions during 4.6 weeks, followed by accelerated fractionation RT using reduced fields, b.i.d., at 1.5 Gy/fraction, with a minimal interval of 6 h between fractions. The total dose was 68.4 Gy in 41 fraction during 6.4 weeks. Patient age, gender, performance score, diet, lesion location, lesion length, stage, and fractionation (CAHF or LCAF) were entered into the univariate and multivariate analyses. RESULTS: All patients finished the treatment course, except for 1 patient in the CAHF group because of severe acute esophagitis. The rate of Grade I, II, and III acute bronchitis was 18.4% (9 of 49), 30.6% (15 of 49), and 8.2% (4 of 49) in the CAHF group and 13.5% (7 of 52), 21.2% (11 of 52), and 3.8% (2 of 52) in the LCAF group, respectively. However, the difference between the two groups was not statistically significant (p = 0.084). The rate of Grade I, II, III, and IV acute esophagitis was 6.1% (3 of 49), 32.7% (16 of 49), 46.9% (23 of 49), and 14.3% (7 of 49) in the CAHF group and 26.9% (14 of 52), 32.7% (17 of 52), 7.7% (4 of 52), and 1.9% (1 of 52) in the LCAF group, respectively. The difference was statistically significant (p < 0.001). The local control rate at 1, 2, and 3 years was 88.7%, 83.9%, and 55.9% in the CAHF group and 80.7%, 71.4%, and 57.1% in the LCAF group, respectively (p = 0.1251). The 1-, 2-, and 3-year survival rate was 79.6%, 51.6%, and 37.6% in the CAHF group and 80.0%, 57.6%, and 41.2% in the LCAF group, respectively (p = 0.5757). Multivariate analysis showed that age and lesion length were independent significant prognostic factors for local control rate, and age was for the overall survival rate. The fractionation schedule had no significant prognostic effect. CONCLUSION: CAHF and LCAF result in similar 1-, 2-, and 3-year local control and survival rates. CAHF resulted in more severe acute esophagitis and may be less well tolerated than LCAF. The treatment results after the CAHF and LCAF regimens were better than those of historical conventional RT.

Adult↗
PubMed2006

Accelerated versus classical hepatitis B virus vaccination programs in healthcare workers accelerated vs. classical HBV vaccination.

BACKGROUND: The aim of this study was to compare the efficacy of a standard hepatitis B virus vaccination program (day 0-30-60) with an accelerated vaccination program (day 0-10-21) in healthy healthcare workers. MATERIAL/METHODS: Participants were randomly assigned to a classical (group 1, days 0, 30, and 60) or an accelerated vaccination program (group 2, days 0, 10, and 21). The vaccine used was 20 pg recombinant hepatitis B vaccine (recombinant hepatitis B vaccine derived from yeast cells, Engerix B, Smith Cline Beachum). HBV markers were re-examined for the emergence of anti-HBsAg and also to detect the development of a possible acute HBV infection one, two, and three months after the last dose of vaccine. Anti-HBsAg titers >10 mIU/l were accepted as protective. RESULTS: The seroprotection rates were similar one, two, and three months after the last dose of vaccine in both groups. Anti-HBsAg titers in group 1 were higher than in group 2 two and three months after the last dose of vaccination (p<0.05). CONCLUSIONS: Our data indicate that the accelerated HBV vaccination program was as effective as the classical vaccination program.

Adult↗
PubMed1980

Acceleration of glomerulonephritis in NZB x NZW mice by early immunization with DNA and injection of bacterial lipopolysaccharide. Experimental approach to the treatment of lupus nephritis by use of the accelerated model of NZB x NZW mouse disease.

The effects of early immunization with DNA and of injection of bacterial lipopolysaccharide (LPS) on the glomerulonephritis of NZB x NZW mice were studied. Combined injections of DNA complexed to methylated bovine serum albumin (DNA-mBSA) and of LPS appeared to be more efficient in accelerating the disease in NZB x NZW mice than injections of DNA-mBSA or LPS alone. A rapid increase in levels of anti-DNA antibodies, an early appearance of severe renal lesions and a shortened survival were observed in mice injected with both DNA-mBSA and LPS. This new model was found to be suitable for therapeutic studies in mice with accelerated disease treated with cyclophosphamide and heparin. The efficacy of cyclophosphamide for the treatment of NZB x NZW mouse disease was shown by immunological and histological studies in mice younger than 4 months. Heparin appeared to have a beneficial effect by preventing the endocapillary cellular proliferation induced by injections of DNA-mBSA and LPS. The accelerated model of NZB x NZW mouse disease might be a useful tool for experiments on the treatment of lupus nephritis.

Animals↗
PubMed1998

FTY720, a novel immunosuppressant, induces sequestration of circulating mature lymphocytes by acceleration of lymphocyte homing in rats. I. FTY720 selectively decreases the number of circulating mature lymphocytes by acceleration of lymphocyte homing.

FTY720, given i.v. or orally at 0.03 mg/kg or more, significantly prolonged skin allograft survival in a dose-dependent manner and showed more potent immunosuppressive activity than cyclosporin A (CsA) or tacrolimus (FK506) in MHC-incompatible rat strains of WKAH donors and F344 recipients. However, unlike CsA or FK506, FTY720 up to 1000 nM did not affect IL-2 production in allogeneic MLC. Within 3 to 24 h after a single oral administration of FTY720 at 0.1 to 1 mg/kg, the number of lymphocytes in the rats was markedly decreased in the peripheral blood and thoracic duct lymph and partially in spleen. By contrast, the number of lymphocytes in peripheral lymph nodes (PLN), mesenteric lymph nodes (MLN), and Peyer's patches (PP) was significantly increased at the same time. Intravenous transfusion of calcein-labeled rat lymphocytes into rats revealed that FTY720 significantly accelerated lymphocyte homing to PLN, MLN, and PP, dose dependently. Since FTY720-induced lymphocyte homing was completely blocked by simultaneous treatment of the calcein-labeled lymphocytes with mAbs against CD62L, CD49d, and CD11a before the transfusion, the acceleration of lymphocyte homing by FTY720 appears to be mediated by lymphocyte-homing receptors. These findings indicate that FTY720 sequesters circulating mature lymphocytes into PLN, MLN, and PP by acceleration of lymphocyte homing and thereby decreases the number of lymphocytes in peripheral blood, thoracic duct lymph, and spleen. Based on these observations, sequestration of circulating mature-lymphocytes is presumed to be a main mechanism of the immunosuppressive activity of FTY720.

Animals↗
PubMed1989

Accelerated bone resorption in senescence-accelerated mouse (SAM-P/6).

Age-associated changes in the femoral bone and in urine and serum composition were studied to understand the low bone mass in a substrain of senescence-accelerated mouse (SAM), SAM-P/6. Age-matched normal SAM-R/1 mice were used as controls. After 13 weeks of age, the concentration of hydroxyproline in the femur of SAM-P/6 was slightly but significantly lower. The urinary excretion rates of cAMP and calcium were higher in SAM-P/6 throughout the whole experimental period, and those of hydroxyproline and phosphorus were higher after 8 weeks. The serum concentrations of calcium and inorganic phosphorus of SAM-P/6 were higher at 13 and 20 weeks. At 5 weeks, the serum alkaline phosphatase and tartrate-resistant acid phosphatase (TRAP) activities of SAM-P/6 were significantly higher. Furthermore, the serum of SAM-P/6 significantly stimulated calcium release from cultured fetal rat ulna. Since urinary cAMP and TRAP in the serum reflect the circulating level of parathyroid hormone and osteoclastic function, respectively, the present results suggest that, in SAM-P/6, accelerated bone resorption produced by a putative hyperparathyroid state causes the decrease in bone mass.

Aging↗
PubMed2000

The autoimmune accelerating yaa mutation does not accelerate murine AIDS.

Murine acquired immunodeficiency syndrome (MAIDS) is characterized by lymphoproliferation, polyclonal B cell activation resulting in the production of autoantibodies, and a progressive immunodeficiency. These are all hallmarks of some autoimmune diseases. Yaa is a Y-chromosome-linked gene that accelerates autoimmune diseases in some autoimmune-prone strains of mice. To further elucidate a possible relationship with autoimmunity, the effect of the Yaa gene on MAIDS was investigated. Analysis of phenotypic and functional disease parameters revealed that Yaa does not accelerate MAIDS disease. This is probably due to the generalized activation of most or all lymphoid cells in MAIDS, which cannot be enhanced by the Yaa gene. This result is in accordance with the selective enhancing effect of the Yaa gene on the immune response against self and foreign antigens in a specific genetic background. It suggests that the autoimmune response associated with MAIDS is a secondary phenomenon. Interestingly, even in wild-type C57BL/6 mice, autoantibody production may contribute overproportionally to the hypergammaglobulinemia associated with MAIDS.

Animals↗
PubMedDate not supplied

Age-related changes in barrier function in mouse brain I. Accelerated age-related increase of brain transfer of serum albumin in accelerated senescence prone SAM-P/8 mice with deficits in learning and memory.

The time course of brain accumulation of radiolabelled human serum albumin ((125)I-HSA) injected intravenously and the transfer of (125)I-HSA from blood to brain were evaluated in DDD mice using a double isotope technique. The brain accumulation of (125)I-HSA at 3 and 9 h but not at 24 h postinjection and the brain transfer rates were significantly higher in 22-month-old DDD mice than in 4-month-old ones. The brain transfer rates of (125)I-HSA were measured also in senescence accelerated prone mice (SAM-P/8) with age-related deficits in learning and memory, and in senescence accelerated resistant mice (SAM-R/I) without these deficits. The brain transfer rates were significantly higher in 13-month-old SAM-P/8 and 22-month-old SAM-R/1 than in 3-month-old mice of the same strains, respectively. The mean brain transfer rates in five regions observed in 22-month-old DDD mice, 22-month-old SAM-R/1 and 13-month-old SAM-P/8 increased by 31%, 41% and 51% compared with corresponding values in 3- or 4-month-old mice of the same strains. DDD mice and SAM-R/1 mice with normal characteristics of aging showed similar age-related significant changes in brain transfer rates. Age-related increase in the brain transfer rate was manifested at the youngest age in SAM-P/8 among the three strains examined. These findings show that the transfer of human serum albumin into the mouse brain increases with aging and suggest that the barrier function in the mouse brain against macromolecules changes with aging.

Journal Article↗
PubMed2006

Transfer of accelerated presbycusis by transplantation of bone marrow cells from senescence-accelerated mice.

Until now, there has been no effective therapy for chronic sensorineural hearing impairment. This study investigated the role of bone marrow cells (BMCs) in cochlear dysfunction. BALB/c mice (2 months of age), a non-presbycusis-prone mouse strain, were lethally irradiated and then transplanted with BMCs from SAMP1 mice (2 months of age), a presbycusis-prone mouse strain. Acceleration of age-related hearing loss, early degeneration of spiral ganglion cells (SGCs) and impairment of immune function were observed in the recipient mice as well as in the SAMP1 mice. However, no spiral ganglion cells of donor (SAMP1) origin were detected in the recipient mice. These results indicated that accelerated presbycusis, cochlear pathology, and immune dysfunction of SAMP1 mice can be transferred to BALB/c recipient mice using allogeneic bone marrow transplantation (BMT). However, although the BMCs themselves cannot differentiate into the spiral ganglion cells (SGCs), they indirectly cause the degeneration of the SGCs. Further studies into the relationship between the inner ear cells and BMCs are required.

Aging↗
PubMed2001

Neurocognitive outcome in brain metastases patients treated with accelerated-fractionation vs. accelerated-hyperfractionated radiotherapy: an analysis from Radiation Therapy Oncology Group Study 91-04.

PURPOSE: To evaluate neurocognitive outcome as measured by the Mini-Mental Status Examination (MMSE) among patients with unresectable brain metastases randomly assigned to accelerated fractionation (AF) vs. accelerated hyperfractionated (AH) whole-brain radiation therapy (WBRT). METHODS AND MATERIALS: The Radiation Therapy Oncology Group (RTOG) accrued 445 patients with unresectable brain metastases to a Phase III comparison of AH (1.6 Gy b.i.d. to 54.4 Gy) vs. AF (3 Gy q.d. to 30 Gy). All had a KPS of >or= 70 and a neurologic function status of 0-2. Three hundred fifty-nine patients had MMSEs performed and were eligible for this analysis. Changes in the MMSE were analyzed according to criteria previously defined in the literature. RESULTS: The median survival was 4.5 months for both arms. The average change in MMSE at 2 and 3 months was a drop of 1.4 and 1.1, respectively, in the AF arm as compared to a drop of 0.7 and 1.3, respectively, in the AH arm (p = NS). Overall, 91 patients at 2 months and 23 patients at 3 months had both follow-up MMSE and computed tomography/magnetic resonance imaging documentation of the status of their brain metastases. When an analysis was performed taking into account control of brain metastases, a significant effect on MMSE was observed with time and associated proportional increase in uncontrolled brain metastases. At 2 months, the average change in MMSE score was a drop of 0.6 for those whose brain metastases were radiologically controlled as compared to a drop of 1.9 for those with uncontrolled brain metastases (p = 0.47). At 3 months, the average change in MMSE score was a drop of 0.5 for those whose brain metastases were radiologically controlled as compared to a drop of 6.3 for those with uncontrolled brain metastases (p = 0.02). CONCLUSION: Use of AH as compared to AF-WBRT was not associated with a significant difference in neurocognitive function as measured by MMSE in this patient population with unresectable brain metastases and limited survival. However, control of brain metastases had a significant impact on MMSE.

Aged↗
PubMed2003

Accelerated aging of senescence accelerated mice R-1 demonstrated by flash visually evoked cortical potentials.

To determine the physiological alterations of visual functions induced by aging, the latency of the N40 peak of the flash visual evoked cortical potentials at several stimulus frequencies were analyzed from senescence accelerated mice (SAM). The senescence prone (P-8) and senescence resistant (R-1) SAM lines were studied. In both the P-8 and ICR (the standard outbred albino laboratory mouse also called CD-1) mice, the peak latency was not significantly different at 6 and 12 months of age. In contrast, there was a prolongation of the peak latency in the R-1 line at 12 months compared to that at 6 months. We conclude that there is an acceleration of the aging process in the R-1 line for visually evoked responses. Thus, the R-1 line might be an independent line suited for the study of aging effects on visual functions.

Aging↗
PubMed2003

Strain rate acceleration yields a better index for evaluating left ventricular contractile function as compared with tissue velocity acceleration during isovolumic contraction time: an in vivo study.

OBJECTIVE: Our study aimed to investigate whether strain rate acceleration (SRA) during isovolumic contraction time (IVCT) could serve as a sensitive indicator of myocardial function. METHODS: A total of 8 sheep underwent occlusion of left anterior descending coronary artery or diagonal branches and 2 sheep underwent left circumflex coronary artery occlusion to create septal, apical, or basal segment myocardial ischemia 19 to 27 weeks before the study. Baseline, volume-loading, dobutamine, and metoprolol infusion were used to produce 4 hemodynamic stages for each sheep. Doppler tissue imaging was acquired using a 5-MHz probe (GE/VingMed Vivid Five, GE Medical Systems, Milwaukee, Wis) on open-chest animals using the liver as a standoff at the apex. Using software (EchoPac, GE Medical Systems), SRA during IVCT was calculated and compared with tissue velocity acceleration (TVA) during IVCT from areas located in the normal and ischemic zones. Also, invasively monitored left ventricle dP/dt was measured as reference contractile function. RESULTS: Both TVA and SRA during IVCT showed higher values for normal tissue than for ischemic area (P <.0001). SRA for normal wall segments changed significantly during the 4 stages (P =.01) with corresponding changes on high-fidelity left ventricular pressure catheters (r = 0.92). TVA over normal segments showed no significant change (P =.29) in the 4 hemodynamic stages. Both TVA and SRA of the ischemic segments showed no significant change with pharmacologic maneuvers or loading conditions. CONCLUSIONS: SRA and TVA during IVCT are both useful indicators for detecting abnormal heart wall motion. However, SRA tends to be more sensitive than TVA for differentiating the response to stress conditions.

Animals↗
PubMed1999

Phospholipase C-beta1 directly accelerates GTP hydrolysis by Galphaq and acceleration is inhibited by Gbeta gamma subunits.

Phospholipase C-beta, the principal effector protein regulated by Galphaq, has been shown to increase the agonist-stimulated, steady-state GTPase activity of Gq in proteoliposomes that contain both heterotrimeric Gq and m1 muscarinic receptor. We now use a moderately stable complex of R183C Galphaq bound to GTP to show that PLC-beta1 acts directly as a GTPase-activating protein (GAP) for isolated Galphaq in a membrane-free system. PLC-beta1 accelerated the hydrolysis of GalphaqR183C.GTP up to 20-fold. The Km was 1.5 nM, which is similar both to the EC50 with which R183C and wild type Galphaq activate PLC-beta1 and to the EC50 with which PLC-beta1 acts as a Gq GAP in the vesicle-based assay. The Galphaq GAP activity of RGS4 can also be quantitated by this assay; it accelerated hydrolysis of bound GTP about 100-fold. The Gq GAP activities of both PLC-beta1 and RGS4 are blocked by Gbeta gamma subunits, probably by a competitive mechanism. These data suggest either that the Gbeta gamma subunits are not continuously required for receptor-catalyzed GDP/GTP exchange during steady-state GTP hydrolysis or that GAPs, either PLC-beta or RGS proteins, can substitute for Gbeta gamma in this set of reactions.

Animals↗
PubMed2000

Modules in the photoreceptor RGS9-1.Gbeta 5L GTPase-accelerating protein complex control effector coupling, GTPase acceleration, protein folding, and stability.

RGS (regulators of G protein signaling) proteins regulate G protein signaling by accelerating GTP hydrolysis, but little is known about regulation of GTPase-accelerating protein (GAP) activities or roles of domains and subunits outside the catalytic cores. RGS9-1 is the GAP required for rapid recovery of light responses in vertebrate photoreceptors and the only mammalian RGS protein with a defined physiological function. It belongs to an RGS subfamily whose members have multiple domains, including G(gamma)-like domains that bind G(beta)(5) proteins. Members of this subfamily play important roles in neuronal signaling. Within the GAP complex organized around the RGS domain of RGS9-1, we have identified a functional role for the G(gamma)-like-G(beta)(5L) complex in regulation of GAP activity by an effector subunit, cGMP phosphodiesterase gamma and in protein folding and stability of RGS9-1. The C-terminal domain of RGS9-1 also plays a major role in conferring effector stimulation. The sequence of the RGS domain determines whether the sign of the effector effect will be positive or negative. These roles were observed in vitro using full-length proteins or fragments for RGS9-1, RGS7, G(beta)(5S), and G(beta)(5L). The dependence of RGS9-1 on G(beta)(5) co-expression for folding, stability, and function has been confirmed in vivo using transgenic Xenopus laevis. These results reveal how multiple domains and regulatory polypeptides work together to fine tune G(talpha) inactivation.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1996

Accelerated senile amyloidosis induced by amyloidogenic Apoa-II gene shortens the life span of mice but does not accelerate the rate of senescence.

The SAMP1 strain is a mouse model for accelerated senescence and severe senile amyloidosis. We studied the effects of the amyloidogenic apolipoprotein A-II gene (Apoa2c) on senile amyloidosis and the life span and progress of senescence of congenic mice (R1.P1-Apoa2c) which have Apoa2c of the SAMPI strain on the genome of the normally aging SAMR1 strain. Age-associated and severe amyloid deposits were detected in R1.P1-Apoa2c, as well as a 20% shorter life span than that of SAMR1. The scores of senescence increased more rapidly with age in R1.P1-Apoa2c than that of SAMR1, and the Gompertz function showed a bigger Y intercept but the same slope of regression line. These results suggest that severe senile amyloidosis induced by the Apoa2c gene shortens the life span of mice but does not accelerate the rate of senescence.

Aging↗
PubMed2000

Wild type ApoA-II gene does not rescue senescence-accelerated mouse (SAMP1) from short life span and accelerated mortality.

Biochemical and genetic data suggest that the Apoa2c allele of the apolipoprotein A-II gene causes severe senile amyloidosis (AApoAII) in SAMP1, a mouse model for accelerated senescence. We analyzed the effects of replacement of Apoa2c in SAMP1 mice with non-amyloidogenic Apoa2b on amyloidosis, lipoprotein metabolism, and progression of senescence using a congenic strain, P1.R1-Apoa2b, which has the Apoa2b chromosome region of SAMR1 in the genome of SAMP1. Age-associated amyloid deposition was not observed, but plasma concentrations of apoA-II protein and HDL-cholesterol decreased with age in P1.R1-Apoa2b. P1.R1-Apoa2b showed lower scores of senescence than did SAMP1. However, the life span and mortality rate doubling time were similar in P1.R1-Apoa2b and SAMP1. These results suggest that replacement of Apoa2c with non-amyloidogenic Apoa2b does not rescue SAMP1 mice from a short life span and accelerated mortality.

Aging↗
PubMed2006

Electron, positron, and photon wakefield acceleration: trapping, wake overtaking, and ponderomotive acceleration.

The electron, positron, and photon acceleration in the first cycle of a laser-driven wakefield is investigated. Separatrices between different types of the particle motion (trapped, reflected by the wakefield and ponderomotive potential, and transient) are demonstrated. The ponderomotive acceleration of electrons can be largely compensated by the wakefield action, in contrast to positrons and positively charged mesons. The electron bunch energy spectrum is analyzed. The maximum upshift of an electromagnetic wave frequency during reflection from the wakefield is obtained.

Journal Article↗
PubMed2005

Hyperfractionated accelerated chemoradiation with concurrent fluorouracil-mitomycin is more effective than dose-escalated hyperfractionated accelerated radiation therapy alone in locally advanced head and neck cancer: final results of the radiotherapy cooperative clinical trials group of the German Cancer Society 95-06 Prospective Randomized Trial.

PURPOSE: To report the results and corresponding acute and late reactions of a prospective, randomized, clinical study in locally advanced head and neck cancer comparing concurrent fluorouracil (FU) and mitomycin (MMC) chemotherapy and hyperfractionated accelerated radiation therapy (C-HART; 70.6 Gy) to hyperfractionated accelerated radiation therapy alone (HART; 77.6 Gy). PATIENTS AND METHODS: Three hundred eighty-four stage III (6%) and IV (94%) oropharyngeal (59.4%), hypopharyngeal (32.3%), and oral cavity (8.3%) cancer patients were randomly assigned to receive either 30 Gy (2 Gy every day) followed by 1.4 Gy bid to a total of 70.6 Gy concurrently with FU (600 mg/m(2), 120 hours continuous infusion) days 1 through 5 and MMC (10 mg/m(2)) on days 5 and 36 (C-HART) or 14 Gy (2 Gy every day) followed by 1.4 Gy bid to a total dose of 77.6 Gy (HART). The data were analyzed on an intent-to-treat basis. RESULTS: At 5 years, the locoregional control and overall survival rates were 49.9% and 28.6% for C-HART versus 37.4% and 23.7% for HART, respectively (P = .001 and P = .023, respectively). Progression-free and freedom from metastases rates were 29.3% and 51.9% for C-HART versus 26.6% and 54.7% for HART, respectively (P = .009 and P = .575, respectively). For C-HART, maximum acute reactions of mucositis, moist desquamation, and erythema were lower than with HART, whereas no differences in late reactions and overall rates of secondary neoplasms were observed. CONCLUSION: C-HART (70.6 Gy) is superior to dose-escalated HART (77.6 Gy) with comparable or less acute reactions and equivalent late reactions, indicating an improvement of the therapeutic ratio.

Actuarial Analysis↗