Calciferol
This drug has not been approved for use by children. Human prostate cells contain receptors for 1a, 25-dihydroxyvitamin D, the active form of vitamin D. Prostate cancer cells respond to vitamin D3 with increases in differentiation and apoptosis, and decreases in proliferation, invasiveness and metastasis. These findings strongly support the use of vitamin D-based therapies for prostate cancer and or as a second-line therapy if androgen deprivation fails. The association between either decreased sun exposure or vitamin D deficiency and the increased risk of prostate cancer at an earlier age, and with a more aggressive progression, indicates that adequate vitamin D nutrition should be a priority for men of all ages. Here we summarize recent advances in epidemiological and biochemical studies of the endocrine and autocrine systems associated with vitamin D and their implications for prostate cancer and in the evaluation of vitamin D3 and its analogs in preventing and or treating prostate cancer. Vitamin D2 ergocalciferol ; is derived from fungi and plants, whereas vitamin D3 cholecalciferol ; is produced in the skin. Both forms referred to here as vitamin D ; are hydroxylated to create the active hormone. The first hydroxylation step, which forms 25 OH ; D see Glossary ; , occurs in the liver. 25 OH ; D then further hydroxylated at the 1a-position by 25 OH ; D-1a-hydroxylase 1a-OHase, also known as CYP27B1 ; in the kidney to form 1a, 25 OH ; 2 D , the active form of vitamin D Fig. 1 ; [1]. The cDNAs that encode 1a-OHase in mice, rats and humans have been cloned [2, 3], and 1a, 25 OH ; 2D is now known to play important roles in the regulation of . 60 genes, including those associated with calcium homeostasis, immune responses, blood pressure control, cell proliferation, differentiation and apoptosis. [1, 3, 4]. Prostate cancer is the most commonly diagnosed and the second most fatal cancer in American men. The inverse correlation P , 0: 0001 between the mortality rate of prostate cancer and exposure to ultraviolet radiation UVR ; in the US population, as well as the greater risk of prostate cancer in Afro-Caribbean men indicate that one precipitating factor for prostate cancer might be vitamin D insufficiency [5]. The biochemical evidence to support a role for vitamin D in prostate cancer includes the demonstration of VDR and the antiproliferative, apoptotic. Patients' accounts of Type 2 diabetes everything for a trial period?' and she [the doctor] said `Well we can certainly give it a try as long as you monitor it fairly closely and if you see it [blood glucose level] creeping up and creeping up then obviously come back and we'll review it'. [Interview 2] Above, Andy describes how medical professionals defer to his expertise in diabetes management. However, Andy acknowledges this expertise is applicable only to his present asymptomatic ; condition. Should the signs such as increased blood glucose levels ; indicate evidence of any deterioration of Andy's condition `if you see it creeping up' ; in the future, then the authority of medicine will once again be bought to bear on the situation. At the third interview, there has apparently been no sign of deterioration to Andy's condition. Here, in response to a question about how he currently feels about his health, Andy marshals evidence from his blood glucose self-monitoring to substantiate the case that currently he has no health problem warranting medical intervention: I don't even consider myself having diabetes you know because the blood sugar has stayed within normal ranges since the first sort of month or two after being diagnosed.while I'm managing it myself then I don't need any real intervention at the moment from anybody else. I don't know how effective the service would be if I wasn't managing it myself or if it was taking a hold you know I couldn't manage it myself. [Interview 3] The success of self-management in Andy's case leads him to speculate that he may not have diabetes currently. Andy does not, however, question the original diagnosis and nor does he assert that things will not change, for the worse, in the future. Although unprepared to speculate on the efficiency of diabetes services at present, he entertains the possibility of a future in which services may be required. contrast to Andy, Sandra represents the extreme position of respondents who described both the cause and management of the condition as outside of their control. When Sandra is asked, `What do you think, if anything, has caused you to get diabetes at this point?' she says: It's hereditary and things like that, or your age like 40 plus they tell you. I thought it was due to the chocolate that I'd been eating but I've since found out it's not--nothing to do with that. It's in your system anyway you know, with what I've been told anyway, being hereditary and stuff like that. [Interview 1] Above, Sandra mobilizes the opinion of `others' to, first, substantiate her current understanding that the onset of the condition is outside of her control, and, second, to absolve her from responsibility and or blame. Although not explicitly citing medical opinion, by referring to `hereditary factors' and `age' she identifies risk factors for the condition accommodated within biomedical explanations. Moreover, in the following extract, Sandra indicates an awareness that lifestyle behaviours as well as medical therapies are important in addressing the condition. However, in response to a question about why she continues to eat chocolate, Sandra juxtaposes lifestyle and medication as two alternative as opposed to complementary ; ways in which she may respond to her diabetes: I'm thinking well, as [my husband] says `Well you don't really want to be on tablets so you'll need to watch yourself and keep it [blood glucose] down'. I says `But if the tablets are going to keep me alive for the rest of my life I'd rather be on them'. [Interview 1] Above, Sandra deploys her husband's words to reflect advice which we might expect to hear from health professionals. That is, by following lifestyle advice she may slow down or halt the progression of the disease which will mean there is less chance that she will need to progress to medication. However, Sandra rationalizes that if medical intervention will ultimately control her condition then, for her, that is the preferred option. Indeed, 5 of 11. Toll-like receptor-2 up-regulates IL-4-induced eotaxin production through signal transducers and activators of transcription STAT ; -6 activation in dermal fibroblasts S Bae, 1 H Murota, 1 I Katayama, 1 Y Sumikawa, 2, 3 S Itami2 and S Akira3 1 Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan, 2 Department of Dermatology, Osaka University Graduate School of Medicine, Osaka, Japan and 3 Research Institute for Microbial Diseases, Osaka University, Osaka, Japan Innate immunity acts as first-line host defense to multi-cellular organisms. Many recent reports have revealed the new roles of toll like receptors TLRs ; in mammalian immune system including TLR-2 mediated activation of mast cells. It is wellknown that CCR3 chemokine, eotaxin plays a central role in the development of Th2 allergic diseases, including atopic dermatitis, asthma, and nasal allergy. To clarify the role of innate immunity in Th2 allergic diseases, we investigated whether TLRs could modulate IL-4 and or TNF alpha -induced eotaxin production by fibroblasts derived from atopic dermatitis patients and TLR mice. As results, eotaxin production and mRNA expression were significantly upregulated in atopic fibroblasts in contrast to normal fibroblasts after IL-4 stimulus. TLR2, 4 and 9 were identified by human fibroblasts at mRNA. Pretreatment of fibroblasts by TLR-2 neutralizing antibody Ab ; inhibited about 30% of eotaxin production and mRNA expression in both fibroblasts. Westhern blot showed that STAT-6 phpsphorylation was also down-regulated in TLR-2 Ab treated fibroblasts, whereas NF kappa B expression was unchanged. Luciferase assay demonstrated TLR-2 Ab treatment had no effect on NF kappa B activation in both fibroblasts stimulated with IL-4 and TNF alpha. To confirm the action of TLR-2 on IL-4 signaling, fibroblasts of TLR-2 mice were stimulated with IL-4 and TNF alpha. TLR-2 mice fibroblast showed a markedly lower STAT-6 expression than wild type after both stimuli. Taken together, our studies provide new evidences that TLR-2 expressed in dermal fibroblasts regulates eotaxin production via STAT-6 signaling. Theses finding could suggest that TLR-2 plays a novel role in Th2 allergic inflammation of the skin, for instance, zinc. Do not use this medication for longer than ten days without your doctor's approval. COCAINE How do cocaine users feel when the drug wears off? and alpha-lipoic. I reluctant to use medicine, so i often use a chinese herb called cordyceps. Herbal calciferolCalciferol vitamin d3Gold Injectables 10 3 2003 SAB-Pharma In response to the recent shortage, SAB-Pharma has started manufacturing and distributing gold sodium thiomalate injection in 1 mL ampoules. Available through normal distribution. Now available. Available from wholesalers as of 1 SAB-Pharma recently acquired this product and reports availability. Related Information Schwarz has discontinued manufacturing of cakciferol No longer available. There are several problems in vitamin D metabolism with advancing age which could increase the requirement for oral vitamin D. First of all, malabsorption of vitamin D occurs in older vs younger people. In a study which used a physiologic amount of vitamin D, it was found that the appearance of tritium labelled cholecalciferol in plasma after an oral dose was diminished in older people as compared to younger people 18 ; . This may be due to decreased numbers of vitamin D receptors in the gut mucosa with advancing age 19 ; . Further, Webb et al have shown that the epidermis and dermis are less able to synthesize vitamin D upon ultraviolet light exposure 20 ; . For example, if the percent of formation of pre-vitamin D free in the 8 year old is considered to be 100%, the 82 year old is only able to synthesize 45% of what the 8 year old is capable of after the same ultra violet light exposure. Further and cordarone. A petechial rash, despite normal platelet count and clotting screen. Skin biopsy did not reveal any clues to aetiology; vasculitis screen was negative. A clinical diagnosis of cutaneous vasculitis was made and he was treated with oral prednisolone with good response. Between 2004 and 2006 he lost 2 stone in weight. He was readmitted in August 2006 with spontaneous haemarthrosis of the right knee, bruising of the shins, ankles and soles of feet, and recurrence of now steroid-resistant ; petechial rash. Dermatology review suggested corkscrew hairs and suggested a re-evaluation of the diagnosis. Methods: Investigations revealed negative vasculitic screen. Clotting screen and echocardiogram were unremarkable. CT chest, abdomen and pelvis and bone scan were unremarkable. He was found to have Vitamin D deficiency 8.7 ug l, 10 deficient, 1030 insufficient, 30 replete ; . Repeat skin biopsy showed normal epidermis with prominent interstitial haemorrhage involving superficial and middermis. MRI of the right knee showed bone bruising and haemorrhage. His multiple vitamin and mineral deficiencies suggested dietary deficiency. Although he was evasive about dietary details, he did admit to having a `typical bachelor's diet', and very poor intake of vegetables or fruit. A clinical diagnosis of Scurvy was made. After discussion with clinical biochemistry it became apparent that measurement of vitamin C is technically very difficult. Treatment with ascorbic acid has shown excellent results with complete resolution of rash and bruising. Oral prednisolone has been withdrawn; he has also been treated with calcium carbonate and ergocalciferol. Results: Privational vitamin C deficiency is a rare diagnosis in the developed world. Scurvy can be readily precipitated by a vitamin C deficient diet e.g. a diet devoid of fruit and vegetables ; , as humans cannot synthesize vitamin C [1]. Studies show clinical deficiency within a month on a vitamin C free diet [2]. Ascorbic acid helps to stabilize the collagen triple helix, and the breakdown of the connective tissue within and supporting the vessel walls is responsible for bleeding [3]. Conclusions: As this case illustrates, scurvy can mimic cutaneous vasculitis, and it is important to recognize this. References. Vitamin d calciferil cholecalciferolThe potential adverse effects of angiotensin on cardiovascular function make its inhibition an attractive therapeutic approach to heart failure. Although ACE inhibitors were designed to decrease circulating and tissue concentrations of A-II, recent evidence suggests that current therapeutic regimens using ACE inhibitors do not adequately suppress A-II production 15 ; . Whether this pharmacologic failure is related to inadequate dosing or frequency of ACE inhibitor administration or to the activity of nonACE-mediated pathways of A-II production 10, 11 ; remains uncertain. The present study raises the possibility that ACE inhibitors are exerting their favorable effects through an alternative mech and endep. A first MI in asymptomatic subjects in the top versus the bottom quintile of cholesterol or CRP levels was less than twofold, while it was more than fivefold in patients in the top quintile of both cholesterol and CRP levels.55 Similarly, in the ECAT study in patients with stable IHD, the risk of MI or death at 18 month follow-up was 0% in patients in the top tertile of total cholesterol levels if they were in the lower tertile of CRP and fibrinogen levels; this percentage rose to 12% for patients in the top tertile of cholesterol, CRP and fibrinogen levels.52 The reasons for the additive or even synergistic prognostic value of cholesterol and CRP levels are still largely unknown; they may lie, however, in the fact that serum cholesterol is an atherogenic stimulus, while CRP is a marker of the degree of the arterial susceptibility to injury. It is worth noting that the intriguing association between CRP and IHD consistently found in prospective studies4854 can be due to confounders. The final evidence of a cause-effect relationship between degree of activation of inflammatory cells and IHD can only come from randomized trials showing that inhibition of inflammatory cell activation results in a reduction of the clinical manifestations of IHD. Susceptibility to risk factors The identification of subjects susceptible to risk factors is a remarkable challenge. However, the recent opportunity of genotyping on a large scale and at low cost can open the way to exciting developments that would have been unthinkable a few years ago. Common variations in genes, called polymorphisms, have been recently associated with the risk of IHD. More importantly, a growing body of evidence indicates that these genetic variations can modulate, by increasing or decreasing, the effect of environmental risk factors on the development of IHD.56 Very promising are the results of some recent studies carried out in Italy. Zito et al., for instance, have shown an interaction between a polymorphism of the gene encoding for the B chain of fibrinogen and seropositivity for Helicobacter pylori in determining the risk of MI. Indeed, carriers of the B2 allele who were seropositive for Helicobacter pylori had a sevenfold increase in the risk of MI as compared to seronegative carriers; conversely, seropositive and seronegative carriers of the B1 allele exhibited a similar risk of MI. These findings underscore the important role of the interaction between environment and genotype in determining clinical events.57 The same group has also shown.
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