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Legislation allowing suitably accredited pharmacists to prescribe within clinical management plans came into th effect on 4 April 2003. The NPC have produced a framework which outlines the competencies that pharmacist supplementary prescribers should acquire during initial training and then maintain. Areas covered are the consultation, prescribing effectively and prescribing in context. The framework may be used for training and development, recruitment and performance review.
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Lachance Y, Luu-The V, Verreault H, Dumont M, Rhaume E, Leblanc G & Labrie F 1991 Structure of the human type II 3 -hydroxysteroid dehydrogenase 5- 4 isomerase 3 -HSD ; gene: adrenal and gonadal specificity. DNA Cell Biology 10 701711. Laughlin GA & Barrett-Connor E 2000 Sexual dimorphism in the influence of advanced aging on adrenal hormone levels: the Rancho Bernardo Study. Journal of Clinical Endocrinology and Metabolism 85 35613568. Laumann EO, Paik A & Rosen RC 1999 Sexual dysfunction in the United States: prevalence and predictors. Journal of the American Medical Association 281 537544. de Launoit Y & Adamski J 1999 Unique multifunctional HSD17B4 gene product: 17 beta-hydroxysteroid dehydrogenase 4 and D-3-hydroxyacyl-coenzyme A dehydrogenase hydratase involved in Zellweger syndrome. Journal of Molecular Endocrinology 22 227240. Leenders F, Adamski J, Husen B, Thole HH & Jungblut PW 1994 Molecular cloning and amino acid sequence of the porcine 17 beta-estradiol dehydrogenase. European Journal of Biochemistry 222 221227. Leiblum S, Bachmann G, Kemmann E, Colburn D & Swartzman L 1983 Vaginal atrophy in the postmenopausal women. The importance of sexual activity and hormones. Journal of the American Medical Association 249 21952198. Levesque E, Turgeon D, Carrier JS, Montminy V, Beaulieu M & Belanger A 2001 Isolation and characterization of the UGT2B28 cDNA encoding a novel human steroid conjugating UDPglucuronosyltransferase. Biochemistry 40 38693881. Li S, Yan X, Blanger A & Labrie F 1993 Prevention by dehydroepiandrosterone of the development of mammary carcinoma induced by 7, 12-dimethylbenz a ; anthracene DMBA ; in the rat. Breast Cancer Research and Treatment 29 203217. Liang T, Rasmusson GH & Brooks JR 1983 12. Androgens: pharmacodynamics and antagonists. Biochemical and biological studies with 4-aza-steroidal 5 -reductase inhibitors. Journal of Steroid Biochemistry 19 385390. Lin SX, Yang F, Jin JZ, Breton R, Zhu DW, Luu-The V & Labrie F 1992 Subunit identity of the dimeric 17 -hydroxysteroid dehydrogenase from human placenta. Journal of Biological Chemistry 267 1618216187. Lindsay R 1993 Hormone replacement therapy for prevention and treatment of osteoporosis. American Journal of Medicine 95 37S39S. Lipworth L, Adami HO, Trichopoulos D, Carlstrom K & Matzoros C 1996 Serum steroid hormone levels, sex hormone-binding globulin, and body mass index in the etiology of postmenopausal breast cancer. Epidemiology 7 96100. Liu H, Robert A & Luu-The V 2005 Cloning and characterization of human form 2 type 17 beta-hydroxysteroid dehydrogenase. A primarily 3 beta-keto reductase and estrogen activating enzyme. Journal of Steroid Biochemistry and Molecular Biology 94 173179. Lobo RA, Rosen RC, Yang HM, Block B & Van Der Hoop RG 2003 Comparative effects of oral esterified estrogens with and without methyltestosterone on endocrine profiles and dimensions of sexual function in postmenopausal women with hypoactive sexual desire. Fertility and Sterility 79 13411352. Lomax P & Schonbaum E 1993 Postmenopausal hot flushes and their management. Pharmacology and Therapeutics 57 347358. Lunglmayr G, Girsch E, Meixner EM, Viehberger G & Bieglmayer C 1988 Effects of long term GnRH analogue treatment on hormone levels and spermatogenesis in patients with carcinoma of the prostate. Urology Research 16 315319. Luu-The V 2001 Analysis and characteristics of multiple types of human 17 beta-hydroxysteroid dehydrogenase. Journal of Steroid Biochemistry and Molecular Biology 76 143151. Luu-The V, Lachance Y, Labrie C, Leblanc G, Thomas JL, Strickler RC & Labrie F 1989a Full length cDNA structure and deduced amino acid sequence of human 3 -hydroxy-5-ene steroid dehydrogenase. Molecular Endocrinology 3 13101312.
Sexual Health Physicians Dr Edward Couglan Dr Jane Morgan Chairperson ; Dr Janet Say NZ Dermatological Society Dr Darian Rowan NZ College of Obstetricians and Gynaecologists Dr Ron Jones Dr Anne Robertson Dr Richard Speed Paediatric Society of New Zealand Prof. Keith Grimwood NZ College of General Practitioners Dr Phil Jacobs Virology Dr Kitty Croxson Family Planning Dr Christine Roke Counselling Catherine Cook Nursing Claire Hurst Georgina McPherson Jessica Crawford Patient Representative Peter Fleming Project Co-ordinator Claire Hurst, PO Box 2437, Auckland Tel: 09 360 1966 Fax: 09 360 2835 Email: info herpes .nz.
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ABSTRACT This was an experimental study using posttest control group design involving Wistar strain Rattus norwegicus as experimental animal. The purpose of this study was to explain the mechanism of BPH in elderly. Samples were randomly divided into 2 groups, 1- and 2-month group, each comprising 26 rats. Each group was divided further into two subgroups, one group received combined estrogen and finasteride, and the other, receiving finasteride only, served as control group. Each subgroup consisted of 13 rats. After treatment for 1 and 2 months, the prostate was removed and examined for TGF-1, EGF, FGF, and proliferation. Immunohistochemistry was used for examining TGF-1, EGF, FGF, and the examination of proliferation was carried out using graticulae. This study employed univariate analysis with 2 sample t test as TGF-1, EGF, and FGF had no correlation. Data analysis used in this research was univariate analysis with 2 sample t test. Analysis result showed that estrogen could reduce TGF-1 significantly in 1 month and 2 month groups p 0.05 ; and estrogen also stimulated significant increase of EGF in 2 month groups p 0.05 ; . Estrogen also increased proliferation significantly in both 1 and 2 month groups p 0.05 ; but estrogen did not increase FGF significantly in both groups. Multiple regression analysis on the effect of TGF-1, EGF, FGF and estrogen to proliferation revealed that only TGF-1 had negative feedback. This indicated that TGF-1 decreased, so that the proliferation increased. Estrogen had positive impact in proliferation, indicating that increased estrogen would also increase proliferation. In conclusion, estrogen increased the proliferation of the prostate cell and EGF significantly and decreased the expression of TGF-1 significantly. This leads to inhibition of proliferation, and finally may cause the occurrence of BPH. Keywords: Prostate, estrogen, TGF-1, EGF, FGF, BPH the influence of androgen and estrogen during aging process, in which there is imbalance between estrogen and testosterone in the prostate Weisser H et al., 1997 ; . Until today, the mechanism of BPH is still debatable. This study was conducted to disclose the mechanism. The results will be useful for improving and developing BPH management. As the prevalence rate of BPH in elderly more than 60 years old ; is high, which is around 67% Sunaryo, 1999 ; , the management of BPH is clearly imperative. Otherwise, the prevalence of obstructive BPH may sharply increase, subjecting the patients to the possibility of having urinary disorder, Lower Urinary Tract Symptoms LUTS ; , sudden dysuria, recurrent urinary tract infection, recurrent hematuria, bladder stones, and renal abnormalities. If it is not adequately managed, it may result in a fatality. In Dr Soetomo Hospital, the annual incidence of BPH requiring operation is 250 cases, occurring mostly in patients aged 60 - 70 years Sunaryo, 1999 ; . Similarly, Berry 1984 ; and Yamanouchi 1994 ; reported that the BPH incidence in patients more than 60 years old was 90%. Several hypothetical explanations have been suggested to explain the mechanism of BPH Kirby et 18 and viagra.
Fisher WA, Rosen RC, Brock G, Karlin G, Pommerville P, Huang XY, Bangerter K, Sand MS, Herman-Gnjidic Z, Derogatis LR. Vardenafil improves treatment satisfaction and sexual pleasure in men with erectile dysfunction and their partners. Fisher WA, Rosen RC, Brock G, Karlin G, Pommerville P, Huang XY, Bangerter K, Sand MS, Herman-Gnjidic Z, Derogatis LR. Vardenafil improves erection quality assessed by the novel erection quality scale in the broad population of men with erectile dysfunction. Greenspan MB, Chang CM. Stable testosterone levels achieved with subcutaneous testosterone injections. Saul D. Sex and the older man Dirty old man? Evaluating the erectile enhancement effect of Andriol Testocaps on senior impotent hypogonadal men. Williams CE, Blunderfield M, Corey JS, Edmonds W, Schallow JR, Amin B, Govedarica S. Psychological and psychiatric classification of men's mental health disorders from the perspective of family practice. Williams CE, Williams HM, Edmonds W, Corey JS, Amin B. Model for a men's health clinic.
Hayles A, Adu D * . Transcultural medicine: race, ethnicity and health. Clin Med 2004; 4 ; : 366-8 Muralidharan V, Imber C * , Leelaudomlipi S, Gunson BK, Buckels JA * , Mirza DF * , Mayer AD * , Bramhall SR * . Arterial conduits for hepatic artery revascularisation in adult liver transplantation. Transpl Int 2004; 17 4 ; : 163-8 Packer C, Stevens A * , Cook A, Raftery J. Diffusion of thrombolysis for acute myocardial infarction from 1981 to 2000 in England: trend analysis and comparison with need. Int J Technol Assess Health Care 2004; 20 4 ; : 531-6 Ward LG, Kendrach MG, Price SO * . Accuracy of abstracts for original research articles in pharmacy journals. Ann Pharmacother 2004; 38 7-8 ; : 1173-7 Kenward G, Castle N, Hodgetts T * , Shaikh L. Evaluation of a medical emergency team one year after implementation. Resuscitation 2004; 61 3 ; : 257-63 Deshmukh SC, Kumar D * , Mathur K, Thomas B. Complex fracture-dislocation of the proximal interphalangeal joint of the hand. Results of a modified pins and rubbers traction system. J Bone Joint Surg Br 2004; 86 3 ; : 406-12 Steeds RP * , Oakley D. Predicting late sudden death from ventricular arrhythmia in adults following surgical repair of tetralogy of Fallot. QJM 2004; 97 1 ; : 7-13 Mant J, McManus RJ, Oakes RA, Delaney BC, Barton PM, Deeks JJ, Hammersley L, Davies RC, Davies MK * , Hobbs FD. Systematic review and modelling of the investigation of acute and chronic chest pain presenting in primary care. Health Technology Assessment 20 Cottrell SM, Morris KP, Davies P * , Bellinger DC, Jonas RA, Newburger JW. Early postoperative body temperature and developmental outcome after open heart surgery in infants. Annals of Thoracic Surgery 2004; 77 1 ; : 66-71; dis Mantry S, Yeung I, Shah S * . Aspheric ablation with the Nidek EC-5000 CX II with OPD-Scan objective analysis. J Refract Surg 2004; 20 5 Suppl ; : S666-8 Walsh AR * , Kombogiorgas D. Coiled ventricular-peritoneal shunt within the scrotum. Pediatr Neurosurg 2004; 40 5 ; : 257-8 Sharma S * , Malarcher AM, Giles WH, Myers G. Racial, ethnic and socioeconomic disparities in the clustering of cardiovascular disease risk factors. Ethn Dis 2004; 14 1 ; : 43-8 Puggioni E, Brignole M, Gammage M * , Soldati E, Bongiorni MG, Simantirakis EN, Vardas P, Gadler F, Bergfeldt L, Tomasi C, Musso G, Gasparini G, Del rosso A. Acute comparative effect of right and left ventricular pacing in patients with atrial fibrillation. Thorne SA * . Pregnancy in heart disease. Heart 2004; 90 4 ; : 450-6 Chaudhari M * , Balmer C, Heng JT, Wright J, Stumper O. Usefulness of BlalockTaussig shunt Doppler flow velocity profiles in the assessment of pulmonary artery pressure and flow. Eur J Echocardiogr 2004; 5 2 ; : 111-7 Hobbs FD, Davis RC, Roalfe AK, Hare R, Davies MK * . Reliability of N-terminal proBNP assay in diagnosis of left ventricular systolic dysfunction within representative and high risk populations. Heart 2004; 90 8 ; : 866-70 Banerjee S * , Denniston AK, Gibson JM, Dodson PM. Does cardiovascular therapy affect the onset and recurrence of preretinal and vitreous haemorrhage in diabetic eye disease?. Eye 2004: Bleetman A, Steyn R, Lee C * . Introduction of the Taser into British policing. Implications for UK emergency departments: an overview of electronic weaponry. Journal of Emergency Medicine 2004; 21 2 ; : 136-40 Evans HM, Sharif K, Brown RM * , Platt C, Crisp WJ, Kelly DA * . Fatal and life threatening rupture of splenic artery aneurysms in children with portal hypertension. Pediatr Transplant 2004; 8 2 ; : 192-5 Cook A, Packer C, Stevens A * , Quinn T. Influences upon the diffusion of thrombolysis for acute myocardial infarction in England: case study. Int J Technol Assess Health Care 2004; 20 4 ; : 537-44 Fitzmaurice DA, Hobbs FD, McManus RJ. Thromboembolism. Fam Physician 2004; 69 1 ; : 132-4 inflammatio n and infection Alaani A, Griffiths H, Minhas SS, Olliff J * , Drake Lee AB * . Parapharyngeal abscess: diagnosis, complications and management in adults. Eur Arch Otorhinolaryngol 2004: Ross J * . Pelvic inflammatory disease. Clin Evid 2004 12 ; : 2259-65 and xanax.
| Testosterone boys and hard liquid girlsStatistical analysis In experiment 1, comparisons of body weight, organ weights and hormone concentrations for the three groups were by analysis of variance and, where significant differences between groups were indicated, sub-group comparisons were by Student's t-test. In experiment 2, any statistical difference between body weight, organ weight and hormone concentrations of the two groups was determined using Student's t-test. The hormone data were also analysed by a second method. The majority of the animals used in these studies were bled before treatment was started, allowing a baseline determination of hormone concentrations. In some instances, pretreatment hormone concentrations were found to be significantly different between control and treated groups. Therefore, hormone concentrations at the various time-points during experiment were also compared with the concentrations present in the pretreatment blood samples for each individual group, using the paired t-test. Mating frequency in control and anastrozole-treated rats was compared using the 2 test. Morphometry data were compared using Student's t-test. Results Efficacy of the route of administration Addition of 200 mg l anastrozole to the drinking water of female rats from postnatal day 21 to day 50 induced a significant reduction in uterine weight, an increase in ovarian weight, a significant increase in peripheral blood concentrations of testosterrone and a modest decrease in blood concentrations of oestradiol Table 1 ; . Plasma FSH concentrations were greater in the anastrozole-treated female rats, but values were not significantly different from those in controls Table 1 ; . Experiment 1 Organ weights Analysis of organ weights in male rats that had been exposed to 100 or 400 mg l anastrozole showed that the only significant difference from controls was in the weights of the testis and ventral prostate: testis weight was significantly increased, whereas ventral.
Due to cirrhosis of liver with encephalopathy.The other deaths have been unrelated to Hepatitis C infections.18 out of 24 patients opted for genotype and viral load study. 5 had less than detectable load of virus.Out of the rest 13, 8 had genotype 1 1a-3 and 1b-5 ; , 4 had genotype 3 3a-3 and 3b-1 ; and 1 had genotype 6 6d 6g ; Conclusion: It was found that the incident of Hepatitis C infection in hemodialysis patients was high 10.21% ; .There was a male preponderance of the patients and they were younger than the patients without infection.Most of the patients had infections at entry to the dailysis unit.Majority of Heaptitis C patients were of the genotype 1 even though genotype 3 is more prevalent in India. Conclusion: Dietary protein intake and dietary energy intake are higher in smaller patients as compared to larger patients. The increase in protein intake is associated with increases of BUN and PCR, which could be interpreted as a high uremic toxin generation induced by protein intake. These findings may be related to increased mortality in patients with small body size and zanaflex!
FIG. 4. NMDA-EPSCs are modulated by androgen treatment in juveniles but not in adults. 5 -Dihydrotestosterone DHT ; pellets were implanted 10 days before recordings made at PHD 45 for DHT-treated juveniles J DHT ; and PHD 100 for DHT-treated adults. Top: average traces from LMAN left ; or RA right ; of NMDA-EPSCs from juvenile J ; , and adults Ad J DHT EPSCs are shown with open circles. Bottom: histograms show the average e-fold decay times mean SE ; for each condition shown above, plus adults treated with DHT; the number of cells in each case is shown in parentheses. Solid bars represent animals treated with DHT; * significantly faster than juvenile controls P 0.05 ; . Androgen treatment did not alter decay times in adults LMAN, P 0.82; RA, P 0.15.
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| When anti-androgens are withdrawn, it is recommended that treatment with LHRHa should continue, as there is evidence they are of benefit, even though theoretically the cancer is no longer androgen-dependent. This is based on two observations. Firstly, tumour cells may become reactivated if testosterpne levels rise again following the removal of a block on their synthesis by the presence of the LHRHa [69, 70]. Secondly, androgen-sensitive cells persist in the treated tumours [70, 71]. Two recent retrospective trials comparing survival times between those who continued androgen deprivation either by means of LHRHa or orchidectomy ; and those who did not, reached opposite conclusions. In one trial, patients had a median survival advantage of 26 months following androgen deprivation [72]; in the other, no survival advantage was demonstrated [73]. However, the retrospective nature of the trials makes definitive interpretation difficult in view of possible selection bias and the absence of stratification of patients by prognostic factors. Results from prospective randomized trials are needed to answer these questions, but general clinical practice is to maintain existing androgen ablation treatment. Despite the fact that androgen-independent cells become more and more prominent, there is a great deal of heterogeneity amongst tumours that have reached the hormone-refractory stage and patients will retain hormone-sensitivity to a greater or lesser extent [74]. In view of this, it is worth considering additional or secondary hormonal manipulations for patients who have failed previous hormonal intervention. This can be approached in different ways. Based on the knowledge that different antiandrogens interact in different ways with the androgen receptor, and have variable half-lives and chemical structures, studies have examined the benefits of employing a second anti-androgen after failure with the first. Some success, as measured by a PSA response, has been found in patients who were given bicalutamide after flutamide withdrawal [75]. The converse situation has not yet been reported. Steroidal anti-androgens, megestrol acetate and cyproterone acetate, can also be used at this point. These drugs achieve an effect in three ways: they competitively block androgen binding to its receptors; they inhibit LH secretion from the anterior pituitary; and they prevent steroidogenesis Fig. 5 ; . A recent trial comparing low-dose and high-dose megestrol acetate in hormone-refractory patients showed an objective response in less than 2% of patients. However 14% of patients had a PSA response, which was associated with a tendency towards improved survival 17.4 months versus 12.7 months ; . The overall median survival was reported as similar to historical controls [76] and zovirax.
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KHC considers third party resources when determining a recipient's eligibility for drug benefits. This may mean that some KHC recipients may not have a drug benefit. KHC does not reimburse for any co-pay co-insurance, for example, boost testosterone.
MEASURE IP OWNER1 NUMERATOR DENOMINATOR asthma medication dispensed, the patient must: meet any one of the other three criteria in step 1, or have at least one diagnosis of asthma in any setting in the same as the leukotriene modifier i.e. measurement year or year prior to the measurement year ; . Medical Record Collection: Electronic Health Record EHR ; users may opt to use this methodology or the electronic data collection methodology described above. EHR users who have information on drugs prescribed and not dispensed may opt to follow the medical record specifications below but produce data on 100% of their denominator population instead of a sample. EXCLUSIONS DATA SOURCE and zyban.
Three most abundant species replaced oleoyl content alone as the measure of muscle LCAC, a value of R2 0.64 was obtained in both cases. In all the above situations, both central fat p 0.002 ; and muscle LCAC p 0.005 ; contributed independently to the multiple regression model. In addition, this key result did not depend on diabetic status; a similar result R2 0.66, p 0.002 ; was obtained when the three diabetic subjects were excluded from the analysis. Again, both central fat p 0.002 ; and muscle LCAC p 0.006 ; remained independent predictors of insulin sensitivity. A stepwise regression analysis, with central fat and muscle LCAC locked into the model, was also performed in an attempt to identify possible additional predictors of insulin sensitivity. Potential predictors were limited to age, indices of diet and physical activity Table 1 ; , diabetic status, glucose tolerance status, and basal plasma concentrations of glucose, cholesterol, HDL cholesterol, NEFA, TG, insulin, C-peptide, testosterone, cortisol, leptin, IL-6, and TNF- . No significant additional terms were found. A second stepwise regression analysis was performed to identify correlates of central fat. The set of potential predictors was that described above, but, in this case, no terms were forced into the regression equation. A univariate model containing only fasting plasma leptin R2 0.41, p 0.006 ; was the outcome. However, this correlation was not site-specific; a stronger relationship existed between plasma leptin concentration and total body fat R2 0.63, p 0.0001 ; . Plasma leptin, by itself, also correlated inversely with insulin sensitivity R2 0.60, p 0.0002 ; , but leptin was not a good substitute for central fat as a predictor of insulin sensitivity when combined with muscle LCAC. In a bivariate analysis, inclusion of muscle LCAC did not significantly p 0.36 ; improve the correlation R2 0.63 ; over that obtained with leptin alone. Simple correlation analyses were also used to investigate possible linking relationships among central fat, insulin sensitivity, and other circulating factors Table 3 ; . Qualitatively, TNF- and IL-6 exhibited a similar pattern to that shown by leptin a positive correlation with central fat and a negative correlation with insulin sensitivity ; , but only the correlation between IL-6 and central fat was statistically significant.
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What must also be understood is that total testosterone alone is not that important, as it is transported through the blood on a carrier molecule known as sex hormone binding globulin shbg.
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