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Dose Treatment (dose + treatment)
Selected AbstractsEffects of estrogen and progesterone treatment on rat hippocampal NMDA receptors: Relationship to Morris water maze performanceJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 4 2004Nahid K. El-Bakri Abstract Estrogen modulates NMDA receptors function in the brain. It increases both dendritic spine density and synapse number in the hippocampus, an effect that can be blocked by NMDA antagonist. In this study, we investigated the effect of 17,-estradiol and progesterone treatment on NMDA receptors in ovariectomized rats. Two different doses were used for 10 weeks. Receptor autoradiography was done on brain sections using [3H] MK-801 as a ligand. Our results showed a significant increase in [3H] MK-801 binding in the dentate gyrus, CA3 and CA4 areas of the hippocampus of ovariectomized compared to sham operated rats. In addition, we observed similar changes in CA1. 17,-estradiol treatment in both doses reduced the binding back to the normal level while progesterone treatment did not show any effect. Spatial reference memory was tested on Morris water maze task. Ovariectomy severely impaired spatial reference memory. Estradiol but not progesterone treatment significantly improved the memory performance of the ovariectomized rats. Low dose treatment showed better learning than high dose estrogen treatment. The decrease in the antagonist sites by estradiol treatment could result in an increase in the sensitivity of the hippocampus to the excitatory stimulation by glutamate system and hence the effect of estradiol on learning and memory. The changes of NMDA receptors in the hippocampus support the concept that estrogen-enhancing effect on spatial reference memory could be through the enhancing of NMDA function. [source] Longitudinal course of depression, fatigue, and quality of life in patients with high risk melanoma receiving adjuvant interferonPSYCHO-ONCOLOGY, Issue 8 2004Peter C. Trask Purpose: Treatment of malignant melanoma with interferon- , has been associated with a variety of side effects ranging from fatigue to depression, and a concomitant impact on quality of life (QOL), in a variety of case reports and cross-sectional clinical trials. Few, if any, studies have been conducted with the express purpose of assessing the longitudinal course of depression, fatigue, and QOL before and during interferon therapy. Description of study: The current study reports on 16 patients who were assessed at 6 points in time: baseline, post high dose, and 1, 2, 3, and 6 months post high dose treatment with interferon- , with the Brief Symptom Inventory, Beck Depression Inventory, Revised Piper Fatigue Scale, and Functional Assessment of Cancer Therapy-Biological Response Modifiers. Results: Results revealed consistent changes from baseline through 6 month assessment. Specifically, increased somatic complaints, depression, and fatigue were observed on the BSI, BDI, and RPFS, respectively. Additional reductions in QOL on the FACT-BRM were also identified. Clinical implications: The findings suggest that IFN has a significant effect on QOL, but that it may be the somatic symptoms of fatigue that contribute to changes on measures of mood. Limiting the amount of fatigue and depression would appear to be significant if individuals are to successfully complete IFN therapy. Copyright © 2003 John Wiley & Sons, Ltd. [source] Short-term treatment using insulin-like growth factor-1 (IGF-1) improves life expectancy of the delta-sarcoglycan deficient hamsterTHE JOURNAL OF GENE MEDICINE, Issue 8 2006Armelle Serose Abstract Background The hamster strain CHF147 presents a progressive dilated cardiomyopathy (DCM) due to a large deletion of the delta-sarcoglycan gene that leads to heart failure. This cardiomyopathy induces premature death. We have previously shown that a short-term treatment using IGF-1 preserves cardiac structure and improves function of the CHF147 hamster. Methods In the current study, we measured long-term effects of short-term treatment with recombinant human IGF-1 (rhIGF-1) in CHF147 hamsters. CHF147 hamsters (7,8 months old) were implanted under the skin with an osmotic pump filled either with saline or with recombinant human IGF-1 at a total dose of 25 µg. The osmotic pump allowed a continuous delivery of the protein for a mean duration of 19 days. Results We observed a significant increase in overall survival, as well as preservation of cardiac function, in the rhIGF-1-treated group. At the time of death, hearts of treated animals did not present any macroscopical or histological differences compared to those of sham hamsters. These results show that rhIGF-1 treatment slows down the evolution of the DCM in the CHF147 hamster. Moreover, the low dose treatment did not increase IGF-1 serum levels. Conclusions This study is the first one reporting beneficial effects of IGF-1 treatment on survival of an animal model presenting DCM. Our results raise hopes for a new therapeutic approach of this pathology. Copyright © 2006 John Wiley & Sons, Ltd. [source] Bayesian Nonparametric Nonproportional Hazards Survival ModelingBIOMETRICS, Issue 3 2009Maria De Iorio Summary We develop a dependent Dirichlet process model for survival analysis data. A major feature of the proposed approach is that there is no necessity for resulting survival curve estimates to satisfy the ubiquitous proportional hazards assumption. An illustration based on a cancer clinical trial is given, where survival probabilities for times early in the study are estimated to be lower for those on a high-dose treatment regimen than for those on the low dose treatment, while the reverse is true for later times, possibly due to the toxic effect of the high dose for those who are not as healthy at the beginning of the study. [source] ORIGINAL ARTICLE: Metabolic outcome of GH treatment in prepubertal short children with and without classical GH deficiencyCLINICAL ENDOCRINOLOGY, Issue 3 2010Ralph Decker Summary Context, Few studies have evaluated the metabolic outcomes of growth hormone (GH) treatment in idiopathic short stature (ISS). Moreover, children with ISS appear to need higher GH doses than children with GH deficiency (GHD) to achieve the same amount of growth and may therefore be at increased risk of adverse events during treatment. The individualized approach using prediction models for estimation of GH responsiveness, on the other hand, has the advantage of narrowing the range of growth response, avoiding too low or high GH doses. Design, Short prepubertal children with either isolated GHD (39) or ISS (89) participated in a 2-year randomized trial of either individualized GH treatment with six different GH doses (range, 17,100 ,g/kg/day) or a standard dose (43 ,g/kg/day). Objective, To evaluate if individualized GH treatment reduced the variance of the metabolic measures as shown for growth response and to compare changes in metabolic variables in children with ISS and GHD. Hypothesis, Individualized GH dose reduces the range of metabolic outcomes, and metabolic outcomes are similar in children with ISS and GHD. Results, We observed a narrower variation for fasting insulin (,34·2%) and for homoeostasis model assessment (HOMA) (,38·9%) after 2 years of individualized GH treatment in comparison with standard GH dose treatment. Similar metabolic changes were seen in ISS and GHD. Delta (,) height SDS correlated with ,insulin-like growth factor I (IGF-I), ,leptin and ,body composition. Principal component analysis identified an anabolic and a lipolytic component. Anabolic variables [,lean body mass (LBM) SDS and ,IGF-I SDS] clustered together and correlated strongly with ,height SDS and GH dose, whereas lipolytic variables [,fat mass (FM) SDS and ,leptin] were clustered separately from anabolic variables. Regression analysis showed GH dose dependency in ISS, and to a lesser degree in GHD, for ,LBM SDS and ,height SDS, but not for changes in FM. Conclusions, Individualized GH dosing during catch-up growth reduces the variance in insulin and HOMA and results in equal metabolic responses irrespective of the diagnosis of GHD or ISS. [source] N -nitrosodimethylamine changes the expression of glutathione S -transferase in the liver of male mice: The role of antioxidantsJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 6 2008S. A. Sheweita Abstract The present study investigated the protective effect of gossypol, selenium, zinc, or glutathione (GSH) against dimethylnitrosamine (DMN)-induced hepatotoxicity in the livers of male mice. The expression and the activity of glutathione S -transferase (GST), levels of GSH, and free radicals (malondialdehyde (MDA)), as well as the activity of glutathione reductase were determined after the treatment of mice for seven consecutive days with low or high doses of gossypol, selenium, zinc, or GSH. In experimental groups, DMN was administered as a single dose for 2 h after the repeated dose treatments of mice for seven consecutive days with each antioxidant. DMN reduced the expression and inhibited the activity of GST. However, repeated treatments of mice with low-dose gossypol or high dose of either selenium or GSH followed by a single dose of DMN induced the expression and the activity of GST. In contrast, low-dose treatments of mice with zinc, selenium, or GSH followed by a single dose of DMN reduced the expression and the activity of GST compared to either control or DMN-treated groups. In addition, high-dose treatment with either gossypol or selenium markedly induced the levels of GSH compared to either control or DMN-treated groups. Interestingly, pretreatment of mice with high dose of either gossypol or selenium for seven consecutive days followed by a single dose of DMN decreased the levels of MDA, whereas DMN induced such levels. It is concluded that high dose of either gossypol or selenium is a stronger protector than zinc and GSH in ameliorating the toxic effects of DMN. © 2008 Wiley Periodicals, Inc. J Biochem Mol Toxicol 22:389,395, 2008; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20255 [source] | ||||||||||