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The relationship between lethality and single radiation dose is usually sigmoidal in shape erectile dysfunction myths and facts discount levitra extra dosage express. Dose-response relationships for normal tissues are generally quite steep and well defined erectile dysfunction causes cancer generic levitra extra dosage 60mg with visa. For study of the response of individual organs erectile dysfunction treatment covered by medicare order generic levitra extra dosage online, one widely used approach is to define a level of functional deficit and to determine the percentage of irradiated animals that express at least this level of damage following different radiation doses. Such results have been reported for specific functional deficits in many tissues. Increased cytokine and chemokine expression has been observed within hours after irradiation when there are no apparent functional or histopathological changes, and may recur and/or persist in cycles over many months. Early increases in cytokine expression can occur after low doses of radiation (~1 Gy) but longer term changes have been observed after larger doses (5 to 25 Gy). In specific tissues they may include other growth factors that are associated with collagen deposition, fibrosis, inflammation, and aberrant vascular growth. These inflammatory factors may induce production of damaging radicals such as reactive oxygen species independently of those caused directly by the radiation treatment. The interplay between these various factors (cell killing, cytokine production, vascular damage) in producing the overall tissue damage remains poorly understood and is likely to vary from one organ to another. Acute tissue responses Acute radiation responses occur mainly in renewal tissues and have been related to death of critical cell populations such as the stem cells in the crypts of the small intestine, in the bone marrow, or in the basal layer of the skin. Responses in these tissues depend on the cell 95 kinetics of the particular tissue but usually occur within 3 months of the start of radiotherapy. They are not usually limiting for fractionated radiotherapy because of the ability of the tissue to undergo rapid repopulation to regenerate the parenchymal cell population and in the case of skin because with high energy beams the dose to the skin surface is less than that at a depth below the basal layer. Radiation-induced cell death in normal tissues generally occurs when the cells attempt mitosis, thus the tissue tends to respond on a time scale similar to the normal rate of loss of functional cells in that tissue and the demand for proliferation of the supporting stem cells. Radiation-induced apoptosis has also been detected in many cells and tissues, such as lymphoid, thymic, and hematopoietic cells, spermatogonia, and intestinal crypts. In lymphoid and myeloid tissue a substantial fraction of the functional cells can die by apoptosis and, thus, this mode of death plays an important role in the temporal response of these tissues to irradiation. In the crypts of the small bowel there is a small fraction of stem cells that die by apoptosis, but the majority dies a mitosis-linked death and the significance of radiation induced apoptosis is unclear. Endothelial cells in the vasculature supporting the crypts and villi of the small intestine of mice have also been reported to be prone to radiation-induced apoptosis, but these reports are controversial. Those cells were reported to be protected by treatment of the animal with basic fibroblast growth factor. This treatment also protected the animals against radiation-induced gastrointestinal injury, suggesting that dysfunction of the vasculature can reduce the ability of the crypts to regenerate. Skin: Following irradiation of skin, there is early erythema within a few days of irradiation and this is believed to be related to the release of 5-hydroxytryptamine by mast cells, increasing vascular permeability. Similar mechanisms may lead to the early nausea and vomiting observed following irradiation of the intestine. Expression of further acute skin reactions (erythema, moist desquamation and ulceration) depends on the relative rates of cell loss and cell proliferation of the basal cells in the epidermis (these cells mature and differentiate to produced the keratinized layers of the skin) and desquamation of the outer skin layers. In human skin this occurs starting at about 2 to 3 weeks into a course of fractionated radiation therapy. The extent of these reactions and the length of time for recovery depend on the dose received and the volume (area) of skin irradiated, because early recovery depends on the number of surviving basal cells that are needed to repopulate the tissue. Erythema in human skin occurs at single doses greater that about 6 Gy, while moist desquamation and ulceration occur after single doses of 20 to 25 Gy. Increased cytokine levels have also been observed in skin and plasma following large doses of irradiation, although their exact role in the observed radiation effects is unclear. Oral mucosa: Oral mucosa has a similar cellular organization to skin but the lifespan of the differentiated cells is shorter so there is more rapid response to irradiation. Many patients may develop spotted-confluent mucositis when doses of 60-70 Gy are delivered in 2 Gy fractions over 6-7 weeks. Similar effects can occur in the oesophagus starting at about 2 weeks into fractionated radiotherapy.

Breast milk from well-nourished mothers in the Nordic countries usually contains sufcient amounts of vitamin A impotence treatments natural levitra extra dosage 60mg with amex. Therefore erectile dysfunction korea cheap levitra extra dosage 40 mg with amex, no specifc recommended intake of vitamin A for infants aged 0?6 months is given erectile dysfunction 2 discount levitra extra dosage 40 mg with mastercard. Any contribution by carotenoids was not considered because the bioconversion of carotenoids in infants is not known. Some early studies (22) found an age-related trend toward higher serum retinol values with advancing age, but recent studies have found trends toward a slight decrease (23). In a Danish cross-sectional study of 80-year-old men and women, 10% had a dietary intake of vitamin A below the lower limit but only one subject had a retinol value below 0. Use of the same vitamin A-containing supplements has been linked to higher circu 340 lating retinyl ester levels in elderly subjects compared to younger subjects (25), and this is due, perhaps, to delayed plasma clearance in the elderly (26). An intervention study found an altered postprandial plasma retinol concentration in older subjects compared to younger, but the intestinal absorption and esterifcation were the same in the elderly compared to the younger subjects (27). Serum retinol levels are generally considered to be a relatively poor refection of vitamin A status unless liver stores are either very depleted or highly saturated but plasma? Several studies (23, 29, 30) have found a positive relationship between plasma levels and the intake of? Upper intake levels and toxicity Several studies have shown that doses up to 180 mg? Adverse efects of dietary retinol need to be considered in Nordic popu lations where the dietary intake of preformed retinol has been relatively high, especially in Iceland. Animal stud ies have shown that retinol serves as an antagonist to vitamin D action, not only in toxic amounts but also at the physiological level (39). In a meta-analysis, which included all cases of retinol intoxication published in the scientifc literature up to the year 2000 (40), it was found that the mean dose of retinol causing hypervitaminosis A was higher when the dose originated from a formula containing vitamin D. This observation implies that there is increased sensitivity for retinol toxicity among subjects with vitamin D insufciency. Risk of acute and chronic hypervitaminosis A Retinol toxicity related to osteoporosis and teratogenicity is discussed in separate sections below. There have been no reports in the Nordic coun tries describing either classical chronic or acute hypervitaminosis A due to intake of foods such as liver except a few cases of early Arctic explorers eating polar bear liver (41). Although adults in the Nordic countries have a generous intake of retinol, very few if any healthy individuals are likely to ingest amounts that might lead to classical hypervitaminosis A. A major issue when evaluating the potential toxicity of retinol is the observation that intake of retinol in various physical forms appears to have diferent thresholds for toxicity (6, 40). Retinol in water-soluble, emulsifed, or solid preparations generally seems to have more acute toxic efects than retinol in foods or oils (40). This might be relevant for potential hypervita minosis A from supplements and from foods fortifed with retinol. If the diet consists of large amounts of retinol-fortifed foods, the daily intake might approach the upper safe levels. Therefore, oil-based retinol preparations should preferably be used in supplements and fortifcation of foods, and supplements and fortifcation with water-miscible and emulsi fed preparations should be kept to a minimum. A total of 17 suspected cases of supplement-induced chronic hyper vitaminosis A, but no acute cases, have been reported in the scientifc literature in the Nordic countries up to 2003 (6). Chronic hypervitaminosis A is induced afer daily doses of 2 mg/kg of retinol in oil-based prepara tions for many months or years (40). Thus, emulsifed/ water-miscible and solid preparations of retinol are about 10 times more toxic than oil-based preparations of retinol. The safe upper single dose of retinol in oil or liver seems to be about 4?6 mg/kg bodyweight (40). Hepatotoxicity is a manifestation of hypervitaminosis A, and toxic symptoms seem to depend on both the amount and duration of exposure. Mechanisms of hepatic efects are linked to overload of the storage capac ity of the liver for vitamin A that can cause cellular toxicity, production of collagen, and eventually fbrosis and cirrhosis in the liver.

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