Home About us Contact | |||
Dose Effects (dose + effects)
Selected AbstractsTime and Dose Effects of Mitomycin C on Extracellular Matrix Fibroblasts and Proteins,THE LARYNGOSCOPE, Issue 1 2005Bryce Ferguson Abstract Objectives/Hypothesis: The objective was to determine treatment dose and time-dependent effects of injected mitomycin C on extracellular matrix fibroblasts, collagen, and fibronectin, important mediators in the wound healing response, in a rat cutaneous wound model. Study Design: A prospective, controlled animal study. Methods: Forty rats were injected with three different doses (0.4, 2.3, and 5.0 mg/mL) of mitomycin C at three different wound sites with a fourth wound site receiving saline as a control. The rats were grouped to have their tissue harvested at five different dates ranging from 1 week to 8 weeks. After death, samples from the wound site underwent Western blot analysis for collagen and fibronectin and histological analysis measuring fibroblast apoptosis. Results: Over an 8-week period, collagen and fibronectin significantly decreased and fibroblast apoptosis significantly increased. No correlation was found between the injected dose of mitomycin C and either the extracellular matrix protein concentration or the rate of fibroblast apoptosis. Conclusion: Mitomycin C demonstrated a long-term effect in a wound, inhibiting collagen and fibronectin production and inducing apoptosis. Use of mitomycin C in excess of 0.4 mg/mL did not alter protein concentrations or rate of apoptosis. [source] Dose effects of the food spice cardamom on aspects of hamster gut physiologyMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 5 2007Ya-Ling Huang Abstract The dose effects of pectic polysaccharide-rich extract from the food spice cardamom (Amomum villosum Lour.) on intestinal environment were investigated. The results showed that pectic polysaccharides and hemicellulose were the major polysaccharides in the cardamom extract. The administration of cardamom extract (0.5 and 1.5 g/100 g diet) effectively (p < 0.05) shortened hamster gastrointestinal transit time by , 58%, increased fecal moisture contents (148,174%), increased SCFA concentrations in hindgut (4.0- to 7.8-fold), decreased the activities of ,- D -glucuronidase (by 71.4,85.7%), ,- D -glucosidase (by 24.3,51.5%), mucinase (by 63.6,72.7%), and urease (by 88.8,90.4%) in feces, and reduced the production of toxic ammonia (by 16.1,64.5%). These findings suggested that the consumption of cardamom extract (at least 0.5 g/100 g diet or 40 mg/day) might exert a favorable effect on improving the gastrointestinal milieu, and also provide a clue to substantiate its traditional therapeutic uses and dosage for intestinal health improvement. [source] Acute Alcohol Effects on Inhibitory Control and Implicit Cognition: Implications for Loss of Control Over DrinkingALCOHOLISM, Issue 8 2010Matt Field Alcohol impairs inhibitory control, and it alters implicit alcohol cognitions including attentional bias and implicit associations. These effects are seen after doses of alcohol which do not lead to global impairments in cognitive performance. We review studies which demonstrate that the effects of alcohol on inhibitory control are associated with the ability of alcohol to prime alcohol-seeking behavior. We also hypothesize that alcohol-induced changes in implicit alcohol cognitions may partially mediate alcohol-induced priming of the motivation to drink. Based on contemporary theoretical models and conceptualizations of executive function, impulsivity, and the motivational salience of alcohol-related cues, we speculate on other aspects of cognition that may underlie alcohol's effects on alcohol seeking. Inconsistencies in existing research and priorities for future research are highlighted, including dose effects and the potential interactions between chronic heavy drinking and the acute effects of alcohol on these cognitive processes. [source] Suppression of adenoviral gene expression in the liver: role of innate vs adaptive immunity and their cell lysis mechanismsLIVER INTERNATIONAL, Issue 3 2005Masahiro Minagawa Abstract Background: Injection of adenoviral constructs causes liver infection prompting immunity, which suppress viral gene expression. Innate and adaptive immunity mediate these processes raising the question which pathways are the most prominent. Methods: Adenovirus expressing the ,-galactosidase (,-gal) gene was injected into normal and immunodeficient mice. Elimination of ,-gal-expressing hepatocytes and increases in liver enzymes were assayed. Major histocompatibility complex (MHC) class I densities, perforin channel insertion and apoptosis by Fas and tumor necrosis factor (TNF)-, were assayed. Results: At high virus doses, suppression of viral gene expression was as efficient in immunodeficient as in normal mice, while at low doses effects of cytotoxic T lymphocytes (CTL) were demonstrable. Despite CTL priming and elimination of infected hepatocytes no liver injury is detected. Hepatocyte MHC I densities were able to trigger CTL granule exocytosis and perforin lysis in vitro but not in vivo. This is we show is because of decreased sensitivity of hepatocytes from infected mice to perforin and increased sensitivity to Fas and TNF-, lysis. Conclusion: Effector cells of the innate immune system are exceedingly effective in suppressing adenoviral gene expression. Perforin-independent pathways, those mediated by TNF-, and Fas are very efficient in hepatocytes from virus-infected livers. [source] |