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Poster 1-1 Poster 1-2 Poster 1-3 Poster 1-4 Poster 1-5 Poster 1-6 Poster 1-7 Poster 1-8 Poster 1-9 Poster 1-10 Poster 1-11 Poster 1-12 Poster 1-13 Poster 1-14 Poster 1-15 Poster 1-16 Poster 1-17 Poster 1-18 Poster 1-19 Patient Variables Predicting Atypical Cytology by Nipple Duct Lavage A choice based conjoint analysis assessing patient preferences for selected features of erythropoietic agents: results in a breast cancer population A Rational Basis for Pathological Sampling of Lymph Nodes in Breast Carcinoma An Update on Prognosis in Breast Cancer Patients with Extensive Axillary Disease Arimided Induced Radiation Recall Dermatitis Atypical lobular hyperplasia and lobular carcinoma in situ: Should they be excised? Bilateral Locally Advanced Inflammatory Breast Cancer BIN 1 and P-Cadherin as prognostic markers for survival in early stage breast cancer Breast cancer and ethnicity: Strong association between reproductive risk factors and Estrogen receptor status in Asian patients Breast Cancer Presenting as Lymphedema of the Arm: A Case Report Breast Retraction Assessment BRA ; of Cosmetic Changes in Patients Undergoing Partial Breast Irradiation: Baseline and Short-term Follow-up Measurements Breast Specific Gamma Imaging : A Clinical Pilot Study Changes in Male Breast Cancer. A 30-Year Review Changing Trends for Mastectomy and Reconstruction Combined Sonographic and Intraoperative Localization with Duct Excision: A Novel Surgical Option in the Managment of Pathological Nipple Discharge DCIS: A Heterogenous Disease with Variable Outcomes Fluorophore-tagged anti-CA 15-3 to improve visualization of breast cancer in-vivo; a potentially useful adjunct for breast cancer surgery Expect the unexpected: Peritoneal spread in relapse of breast cancer Extrammamary Paget's Disease of the Axilla: An Unusual Case.
ICD-9-CM Coordination and Maintenance Committee Meeting March 22-23, 2007 TABULAR MODIFICATIONS V07 New subcategory Need for isolation and other prophylactic measures V07.4 Prophylactic use of agents affecting estrogen receptors Prophylactic use of hormone therapy Use additional code to identify: estrogen receptor positive status V86.0 ; family history of breast cancer V16.3 ; genetic susceptibility to cancer V84.01-V84.09 ; personal history of breast cancer V10.3 ; postmenopausal status V49.81 ; New code V07.41 Prophylactic use of selective estrogen receptor modulators SERMs ; Prophylactic use of: raloxifene Evista ; tamoxifen Nolvadex ; toremifene Fareston ; Prophylactic use of aromatase inhibitors Prophylactic use of: anastrozole Arimixex ; exemestar Aromasin ; letrozole Femara ; Prophylactic use of other agents affecting estrogen receptors Prophylactic use of: estrogen receptor downregulators fulvestrant Faslodex ; gonadotropin-releasing hormone GnRH ; agonist goserelin acetate Zoladex ; leuprolide acetate leuprorelin ; Lupron ; megestrol acetate Megace.
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AMLODIPINE BESYLATE rdiovascular system.116 .Repatriation Schedule.408 AMMONIUM CHLORIDE.148 Amohexal HX ; .Antiinfectives for systemic use .157, 158 ntal .289, 290 AMOROLFINE HYDROCHLORIDE .Repatriation Schedule.410 Amoxil GK ; .Antiinfectives for systemic use .157, 158 ntal .289, 290 Amoxil Duo GK ; .159 Amoxil Forte GK ; .Antiinfectives for systemic use .158 ntal .290 AMOXYCILLIN .Antiinfectives for systemic use .157, 159 ntal .289 AMOXYCILLIN with CLAVULANIC ACID .Antiinfectives for systemic use .162 ntal .293 Amoxycillin Sandoz BG ; .159 Amoxycillin-BC BG ; .Antiinfectives for systemic use .157, 158 ntal .289, 290 Amoxycillin-DP DG ; .Antiinfectives for systemic use .157, 158 ntal .289 AMPHOTERICIN .Alimentary tract and metabolism .69 .Antiinfectives for systemic use .173 ntal .285 AMPICILLIN .Antiinfectives for systemic use .159 ntal .290 Amprace 5 AD ; .120 Amprace 10 AD ; .121 Amprace 20 AD ; .121 AMPRENAVIR ction 100.312 Anafranil 25 NV ; .233, 235 Anamorph FM ; ntal .304 .Nervous system .215 Anandron AV ; .188 Anaprox 550 RO ; ntal .302 .Musculo-skeletal system .206 ANASTROZOLE .188 Andriol OR ; .137 Androcur SC ; .Antineoplastic and immunomodulating agents .188 .Genito urinary system and sex hormones .147 Androcur-100 SC ; .Antineoplastic and immunomodulating agents .188 .Genito urinary system and sex hormones .147 Androderm MX ; .137 Anginine Stabilised SI ; rdiovascular system.107 ntal .287 Anpec 40 AF ; .117 Anpec 80 AF ; .117 Anpec SR AF ; .118 Anselol 50 mg DP ; .113 ANTAZOLINE with NAPHAZOLINE .Repatriation Schedule.427 Antenex 2 AF ; ntal .308 .Nervous system .232 Antenex 5 AF ; ntal .309 .Nervous system .232 Anthel 125 AF ; .248 Anthel 250 AF ; .248 Antistine-Privine NV ; .Repatriation Schedule.427 Antroquoril EX ; .132 Anusol WW ; .Repatriation Schedule.408 Anzatax MX ; .182 Anzemet AV ; .77 Apomine MX ; ction 100.312 APOMORPHINE HYDROCHLORIDE ction 100.312 Apoven 250 DP ; .254 Apoven 500 DP ; .254 APRACLONIDINE HYDROCHLORIDE .260 Aprinox AB ; .110 Aquacare H.P. AG ; .Repatriation Schedule.411 Aquacel 177902 CC ; .Repatriation Schedule.438 Aquacel 177903 CC ; .Repatriation Schedule.438 Aquacel 177904 CC ; .Repatriation Schedule.438 Aquae HA ; .Palliative Care.277, 278 .Repatriation Schedule.404 Aquasun Lotion SPF 18 PF ; .Repatriation Schedule.411 Arabloc HP ; .201 Aranesp AN ; ction 100.324 Aratac 100 AF ; .106 Aratac 200 AF ; .106 Arava AV ; .200, 201 Aredia 15 mg NV ; .Musculo-skeletal system .210 ction 100.325 Aredia 30 mg NV ; .Musculo-skeletal system .210 ction 100.325 Aredia 90 mg NV ; ction 100.325 Aricept PF ; .241 Arima AF ; .238 Arima 300 AF ; .238 Aarimidex AP ; .188 ARIPIPRAZOLE .230.
PROSTASCINT To date, PROSTASCINT monoclonal antibody has been safely used in over 60, 000 patients, establishing a clear clinical experience. The full extent of PROSTASCINT's potential is equally apparent in the growing number of new opportunities that reach beyond the product's current diagnostic capabilities. Already the first and only FDA approved agent for prostate specific imaging, PROSTASCINT is being evaluated in areas that include a variety of image-guided applications in brachytherapy, intensity modulated radiation therapy IMRT ; --currently in combination Phase I II study--and cryotherapy. For new opportunities with more far reaching implications, PROSTASCINT is also being studied as a response monitoring tool in certain cytotoxic therapies, and for use as a highly accurate imaging agent in other cancers, which may one day help enable more effective treatment outcomes. Looking ahead, we expect that near term growth will come from the greater awareness of PROSTASCINT outcomes data and the increasing standardization of fusion imaging use at major facilities. As part of our growth strategy for PROSTASCINT, Cytogen has focused our sales and marketing efforts on expanding the use of newer and more accurate fusion imaging technologies, educating radiation and oncology specialists about the added value that these new technologies bring to their patients and their practices. A number of recent studies support the direction we've taken, including one study of 49 patients, where PROSTASCINT demonstrated a surgically confirmed 83 percent accuracy, while localization accuracy doubled with the use of fusion images. A number of study results presented in 2005 validated the effectiveness of PROSTASCINT in response monitoring and patient outcomes. In one study of 239 patients, PROSTASCINT fusion imaging was used to define biological targets for brachytherapy, which resulted in disease free survival rates superior to standard implant techniques in low, intermediate, and high risk patients and danazol.
Ternating hypertonia and hypotonia; dystonic posturing of the arms ; becoming more and more apparent. The characteristic odor of the urine, described as smelling like maple syrup, burnt sugar, or curry, is then noted. Finally, seizures and coma, leading to death in untreated cases ; , occurs.109 Laboratory findings include increased concentrations of BCAAs, ketosis, acidosis, and occasionally hypoglycemia.114 Patients with intermittent MSUD enzyme activity 5%20% ; exhibit normal growth and intelligence. These children do not go into metabolic crisis unless the body is in a stressful situation, such as an infection ie, otitis media ; or after surgery.115 Although patients with intermittent MSUD generally present between 5 months and 2 years of age secondary to a minor infection, some individuals have not shown symptoms until the fifth decade. Concentrations of BCAAs are normal between episodes. In contrast, patients with intermediate MSUD enzyme activity 3%30% ; do not present with catastrophic illness during the neonatal period but have gradual neurologic problems, eventually resulting in mental retardation. In one study, most were diagnosed between 5 months and 7 years of age while undergoing evaluation for developmental delay or seizures.116, 117 Several patients have had episodes of ketoacidosis, but acute encephalopathy is rare.118 Increased concentrations of BCAAs and BCKAs in serum and urine are present. Patients with thiamine-responsive MSUD enzyme activity 2% 40% ; have a clinical course similar to those with intermediate MSUD. These patients have decreased concentrations of BCKAs and or BCAAs with thiamine therapy in varying dosages ranging from 10 to 1000 mg day.119, 120 In some instances, the patient does not show the full response to thiamine until therapy has commenced for 3 weeks.121 In all documented cases, patients required dietary intervention in conjunction with thiamine to achieve metabolic control.109 E3-deficient MSUD E3 deficiency ; is rare, with fewer than 20 patients having been described.109, 122, 123 Clinically, newborn infants with E3 deficiency are similar to patients with intermediate MSUD, but severe lactic acidosis is also present. The infants develop a persistent lactic acidosis between 8 weeks and 6 months of age followed by progressive neurologic deterioration with hypotonia, developmental delay, and movement disorder. Laboratory findings include mild to moderately increased concentrations of BCAAs and increased lactate, pyruvate, -ketoglutarate, -hydroxyisovalerate, and -hydroxyglutarate concentrations. The patients have a combined deficiency of BCKD, pyruvate, and -ketoglutarate dehydrogenase complexes, leading to the more complex phenotype. Various combinations of dietary therapy, vitamin therapy thiamine and biotin ; , and lipoic acid have been tried without success.122.
| Arimidex 1mg tabletNatbcc ; . Their opinion was echoed within days in an October 12 editorial in the New York Times, which questioned whether scientists were engaging in "ethical overkill" by halting the study midstream. The NBCC's position is that patients were followed for much too short of a time--an average of just 2.4 years-- and that the way recurrence was measured was not meaningful because local and metastatic Dr. Jeffrey Abrams recurrences of breast cancer were considered together with new primary cancers in the contralateral breast--cancers that have different risk profiles and treatment options. "The issue to us is long-term survival--is this drug really going to save lives?" asked NBCC president Fran Visco. "What are the long-term effects, and how do you balance those against what the benefits are? We really don't know because it was stopped so early." To Susan Love, M.D., the unanswered question of long-term side effects will make it difficult for women to decide whether they should use letrozole and for how long. Love, president and medical director of the Susan Love, M.D., Breast Cancer Foundation, said that many women using the drug will experience an adverse effect on quality of life, while few will benefit. The results "weren't strong enough" to suggest widespread use of the drug, especially since aromatase inhibitors like Qrimidex anastrozole ; have already been shown to cause musculoskeletal problems, said and femara!
H Dublin called for success stories since WCC 3.2, and the SC members gave them as follows: J Smart said that during this week we have had 6-times as many website hits as usual. She also mentioned that a colleague at HQ had asked that JC give his successful "brown bag lunch" on Red Listing to the IUCN Council. ; M Samways commented on the removal of aliens and recovery of water resources, and how by using the Biotic Recovery Index ; two species of Damsel Flies have returned on Table Mountain. Y Sadovy commented that with regards to species on the CITES Appendices within a year from the listing, we have gone from a situation whereby a CITES listing for fish was so new that authorities could not decide what to do, to a situation to where the Indonesian Government is collaborating with an IUCN Specialist Group ; on censusing towards nondetriment findings for the Napoleon wrasse. R Kock commented on the anthrax outbreak recently reported from Northern Kenya affecting endangered Grevy's zebra. The managers of the problem on the ground had benefited from IUCN SSC support in bringing information and experts together to advise. The rapid attention to the problem which led to vaccination of Grevy's zebra is a model for intervention, although the real impact on this disease needs to be evaluated and this recent case in Kenya has provided a rare opportunity. There have been a series of anthrax events in Africa such as the discovery of anthrax in chimps ; and the apparently increasing frequency of outbreaks in other game species may relate to changing livestock management and reduced veterinary capacity on the continent i.e. reduced vaccination coverage ; . Other factors like climate change also need to be considered as possible drivers for re-emergence of this disease. S Stuart noted that an NGO in Colombia looked at the Global Amphibian Assessment website and found there were many species on a certain mountain, so they purchased some private land there to safeguard these species. C Gascon, Co-Chair of the Amphibian SG, has helped Colombian herpetologists in this regard. S Stuart also noted that there are six endemic frogs in a forest in Sri Lanka, and there are plans to buy portions of land for the Forestry Department to run. R Pethiyagoda is involved. H Dublin mentioned that an important aim of the SSC is to be more responsive to the recommendations of the 2001 Voluntarism Study. One issue raised was the need for greater individual recognition for contributions made to SSC. To this end, the last issue of Species highlighted SG Chairs, asking them to provide their own written profile and photo. This has been well received and therefore we are going to continue to do the others in the next issue.
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Occurs with the accumulation of tenofovir in the proximal tubule and appears to be concentration dependent.2 Cases of renal failure with tenofovir have been reported in patients with no known risk factors.1 However, published case reports of nephrotoxicity suggest that there may be specific risk factors for the few patients in whom tenofovir-related nephrotoxicity develops.2 Risk factors may include pre-existing renal dysfunction, long duration of use, low body weight, concomitant use of drugs and mircette.
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ANASTROZOLE Restricted benefit Treatment of hormone-dependent advanced breast cancer in post-menopausal women; Treatment of hormone-dependent early breast cancer in post-menopausal women in whom tamoxifen citrate therapy is contraindicated; Treatment of hormone-dependent early breast cancer in post-menopausal women who are intolerant of tamoxifen citrate. NOTE: This drug is not PBS-subsidised for primary prevention of breast cancer. 8179L Tablet 1 mg 30 2 . 217.09 28.60 Aromidex AP.
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4.06 and 35.43 8.40 in both groups, respectively. A second heart rate variability assessment was available in 120 175 patients 69% ; after three months. Serial measurements in this subgroup revealed that after three months, heart rate variability had increased both in patients with index of less or equal to 25 ; and patients without index of more than 25 ; a reduced heart rate variability at discharge. However, the increase in heart rate variability was more pronounced in patients with an index of less or equal to 25 increase 11.16 7.37 versus 5.97 12.14, p 0.004 ; . After three months, 31 120 25% ; patients who had an index of less or equal to 25 at discharge showed an improvement to an index of more than 25 and 5 120 4% ; patients with an index of more than 25 at discharge had a worsening of their index to of less or equal to 25. All other patients remained in the same category as they were at discharge 70 120 58% ; with an index of more than 25 and 14 120 11% ; with an index of less or equal to 25 ; . Echocardiography.
Activities were biphasic in nature although the basis of the nonlinear results has not been established. Two apparent Ki values were exhibited by anastrozole for inhibition of CYP1A2 and CYP3A metabolism. The low Ki values for these two enzymes was similar to the single apparent Ki determined for inhibition of CYP2C9 activity by anastrozole Ki 8 -10 M corresponds to 2.3 to 2.9 g ml 1 ; . The low Ki values were used to estimate conservatively the potential for inhibitory drug interactions with anastrozole during clinical use of the drug. Average steady-state Cmax concentrations in patients chronically administered the 1-mg marketed dose of Arimidex were approximately 0.08 g ml 1 0.3 M ; . These plasma concentrations are 30-fold lower than the apparent Ki values determined in these in vitro studies, suggesting that anastrozole would cause little or no inhibition in vivo of the metabolism of drugs that are substrates for CYP1A2, CYP2C9, and CYP3A enzymes per cent inhibition in vivo predicted to be approximately 3% ; . Although a lack of inhibition potential can be predicted from these in vitro results, any effect of intracellular binding or accumulation of anastrozole in hepatocytes on the in vivo inhibition have not been accounted for in these investigations.3 Nifedipine oxidation in human liver microsomes was not decreased by two major metabolites triazole and BMPN-benzoic acid ; of anastrozole at concentrations up to 250 M. The lack of CYP inhibition by these metabolites is consistent with requirement for both hydrophobic character for active site access and the heteratomic lone pair of electrons in triazole for Type II binding to the heme iron 23 ; . The results herein also show that the ability of anastrozole to inhibit drug metabolizing CYP enzymes in liver microsomes is much weaker than the inhibition of aromatase. When comparing the IC50 for inhibition of human placental aromatase activity 15 nM ; with the inhibition of the hepatic microsomal CYP produced by anastrozole in vitro, a margin of selectivity of at least 500-fold is obtained. In conclusion, the results of the in vitro experiments performed in human liver microsomes indicate that, although anastrozole can inhibit CYP1A2, 2C9, and 3A-mediated catalytic activities, the level of inhibition in vivo during clinical therapy with Arimidex Zeneca, Ltd., Macclesfield, UK ; 1-mg would not be expected to cause clinically significant interactions with other CYP-metabolized drugs and zelnorm.
Anti-HIV medicines. What your maxienough of the medicine in your body This supplement was the brainchild of mal effect may be, however, is also incorrect dosing or poor adherence ; the late editor of Positively Aware, dependent on your history of taking could result in either toxic effects or no Charles Clifton. Charles and I met in HIV medicines and how much damage effect. Neither of these are desired out appropriately enough ; San Francisco, the virus has already done to your comes -- for you or your doctor! The during the Retrovirus conference in body. You and your doctor should have paragraph below provides a more 2004 to discuss ways to educate talked about what the goals for your detailed explanation of the graph. It is patients about how their body breaks drugs are before you started taking important to understand these condown medicines. The intent of this supthem. Not everyone can or should use cepts, as they are pivotal to the inforplement is to provide foundational genan undetectable viral load and "normal" mation provided in this supplement. eral knowledge about the pharmacokiT-cell count as goals. The drug concentration in the netics and pharmacodynamics see If the drug you take is not in sufblood rises as you go from left to right ABC's of Antiretrovirals ; of antiretrovificient quantity, you can get sub-optialong the x-axis or bottom of the graph. ral medications. It also gives specific mal levels. At this drug concentration, The actual amount milligrams per milrecommendations on currently availyou would likely not see a able medicines. Why does your therapeutic good ; benefit doctor prescribe Lexiva once a AND from taking the medicine. day for you and twice a day for SHOULD HAVE TALKED ABOUT WHAT Even though you don't get a your partner? Why do you have to positive effect, you can still eat with Reyataz and cannot eat FOR YOUR DRUGS ARE THE see a negative one. For with Crixivan? Why is Videx EC BEFORE YOU STARTED TAKING THEM instance, taking low doses of given sometimes at 250 mg and Retrovir will not change your sometimes at 400 mg daily? These viral load or T-cells, but may still cause liliter of blood, see ABC's of Pharmacowere just some of the questions Charles you to have anemia. kinetics ; varies depending on several and I hoped to be able to answer with If too much medicine is taken, factors including: the drug, prescribed this supplement. then the chance that you will have a dose, how long you have been taking How much milligrams ; of a toxic effect becomes more likely. An the medicine and how long it has been drug should be taken at one time? example of this is taking too much since you took your last dose. The The answer most often times is: Crixivan. Very high levels of Crixivan chance of the drug having an effect enough to work, but not too much to can cause you to develop stones in increases up to a maximal amount as cause significant side effects. Most your kidneys very painful! ; . Not only you go from bottom to top or up the yantiretrovirals are dosed to achieve in is this drug's recommended doses axis. As stated previously, for antiretrothe body a level of drug that falls into from the company and in this supplevirals this effect is measured by changes what is called a "therapeutic range" ment -- see Protease Inhibitors ; at levin T-cell count and viral load. You prob see Figure 1: Therapeutic Range ; . els that usually don't allow this to hapably know that the most you can Taking enough of the medicine havpen, drinking plenty of water immedireduce your viral load is down to less ing drug concentrations somewhere on ately after the dose and during the day than 50 copies per milliliter -- so there the graph ; will, in most cases, give you help minimize this risk is a maximal effect the drug can have an effect. These effects can be good The challenge with HIV medion your virus. Same with T-cells -- therapeutic ; or bad toxic ; . cines is that the "therapeutic range" in your body can only make so many over If the drug level is appropriate for many instances is still being discovered. time and at some point you will have Tthe virus in your body, you could see a What is the maximum level of drug that cells in the "normal" or non-HIV infectlowering of the viral load and or should be in the body daily to provide ed range. These two levels undeincreasing of the CD4 count. These long term therapeutic effects? Sadly, tectable viral load and normal CD4 would obviously be good therapeutic this is not known for every drug. What count ; represent a maximal effect of the effects. Taking too much or not having.
Korovin, E. P, 1961. Vegetation of Middle Asia and southern Kazakhstan. Uzbekistan Academy of Science Press, Tashkent, USSR in Russian ; . Krasnov, B., and T. Kniazeva. 1983. Ectoparasite exchange between midday jird, Meriones meridianus, and house mouse, Mus musculus, by direct contacts, pp. 243-244. In Y. Suchkov and I. Taran [eds. ], Proceedings of Conference on Prophylactics of Diseases in Natural Foci. Caucasus Anti-Plague Institute, Stavropol, USSR in Russian ; . Krasnov, B and G. Shenbrot. 1996. Spatial structure of community of darkling beetles Coleoptera: Tenebrionidae ; in the Negev Highlands, Israel. Ecography 19: 139152, Krasnov, B. R., G. I. Shenbrot, I. S. Khokhlova, and E. Y. Ivanitskaya. 1996a, Spatial patterns of rodent communities in the Ramon erosion cirque, Negev Highlands Israel ; . J. Arid Environ. 32: 319-328. Krasnov, B. B G. I. Shenbrot, I. S. Khokhlova, A. A. Degen, and K. V. Rogovin. 1996b. On the biology of Sundevall's jird Meriones crassus Sundevall, 1842 ; Rodentia: Gerbillidae ; in the Negev Highlands, Israel. Mammalia 60: 375-391, Krasnov, B. R., G. I. Shenbrot, S. G. Medvedev, V. S. Vatschenok, and I. S. Khokhlova. 1997. Host-habitat relations as an important determinant of flea assemblages Siphonaptera ; on rodents in the Negev Desert, Parasitology 114: 159-173. Kuris, A. M, A. R. Blaunstein, and J. J. Aho. 1980. Hosts as islands. Am. Nat. 116: 570-586. Nativ, R., and E. Mazor. 1987. Rain events in an arid environment--their distribution and ionic and isotopic composition patterns: Makhtesh Ramon basin, Israel. J. Hydrol, 89: 205-237. Nazarova, I. V. 1981. Fleas of Volga-Kama region. Nauka, Moscow, USSR in Russian ; , Osborn, D, J., and I. Helmy, 1980. The contemporary land mammals of Egypt including Sinai ; . Fieldiana Zoology 5: 1-579. Pavlinov, I., Y. Dubrovsky, O. Rossolimo, and E. Potapova. 1990. Gerbils of the world. Nauka, Moscow, USSR in Russian ; , Pielou, E, C. I9S4. The interpretation of ecological data. Wiley, New York, Pimm, S. L., and M. L. Rosenzweig. 1981. Competitors and habitat use. Oikos 37: 1- 6. Price, P. W. 1977. General concepts on the evolutionary biology of parasites. Evolution 31: 405-420. 1990. Host populations as resource defining parasite community organization, pp. 21-40. In G. Esch, A, Bush, and J. Aho [eds], Parasite communities: patterns and processes. Chapman & Hall, London. Sapegina, V. F and A. G. Reitblat. 1981. Distribution of flea Ceratophyllus tesquorum Wagn., 1898 in Terek-Kuma interfluve, pp, 177-181. In A. Maximov [ed, ], Biological problems of diseases in natural foci. Nauka, Novosibirsk, USSR in Russian ; . Stanko, M. 1994. Fleas synusy Siphonaptera ; of small mammals from the central part of the East-SIovakian lowlands. Biologia Bratisl. ; 49: 239-246. Theodor, O., and M. Costa 1967. A survey of the parasites of wild mammals and birds in Israel. I ; Ectoparasites. Israel Academy of Science and Humanities, Jerusalem. Trpis, M. 1994. Host specificity and ecology of fleas Siphonaptera ; of small mammals in mountains of North-Central Slovakia. Bull. Soc. Vector Ecol. 19: 18-22 and levlen.
The desired agent. Production costs are low, and aerosol dispersal equipment from commercial sources can be adapted for biologic weapon dissemination. Bioterrorists operating in a civilian environment have relative freedom of movement, which could allow them to use freshly grown microbial suspensions storage reduces viability and virulence ; . Moreover, bioterrorists may not be constrained by the need for precise targeting or predictable results. The impact of a bioterrorist attack depends on the specific agent or toxin used, the method and efficiency of dispersal, the population exposed, the level of immunity in the population, the availability of effective postexposure and or therapeutic regimens, and the potential for secondary transmission. Understanding and quantifying the impact of a bioterrorist attack are essential to developing an effective response. Therefore, we have analyzed the comparative impact of three classic biologic warfare agents Bacillus anthracis, Brucella melitensis, and Francisella tularensis ; when released as aerosols in the suburbs of a major city and compared the benefits of systematic intervention with the costs of increased disease incidence from the economic point of view used in society.
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Aromatase inhibitors arimidex ; aromatase inhibitors are commonly used by men who are using 5 alpha reductase inhibitors and worried about feminizing effects such as gyno.
What is Arimidex? Arimidex is the first in a class of selective non-steroidal, anti-oestrogen, hormonal endocrine ; prescription medicines known as aromatase inhibitors, or `AIs'. How is Arimidex administered? Arimidex is administered via a once-daily oral 1mg tablet. How does Arimidex work? In postmenopausal women, the ovaries no longer produce oestrogen. Instead, the hormone is produced in small quantities by a process known as `aromatisation' in other tissues such as fat, muscle and the liver. In cases of breast cancer, the breast tumour itself also produces oestrogen. Aromatisation depends on the activity of the aromatase enzyme. Arimidex works by disrupting this process. By inhibiting the production of oestrogen, Arimidex starves the tumour of its main nutrient and, therefore, prevents the cancer's growth. What is Arimidex licensed for and where? Arimidex is approved in over 80 countries including the US, UK, France, Germany, Italy and Spain ; for the adjuvant treatment of postmenopausal women with hormone-receptor positive early invasive breast cancer Arimidex is approved worldwide for the treatment of postmenopausal women with hormonereceptor positive advanced breast cancer Please note: the specific license indication may vary in different countries. Arimidex is the only treatment in its class to be licensed worldwide for both initial adjuvant therapy and switching from tamoxifen for those patients who are already being treated with tamoxifen ; . Arimidex is also the only AI that has been proven to benefit women in the three stages of early breast cancer treatment initial adjuvant, immediate switching from tamoxifen and extended adjuvant ; . What data are there to support the use of `Arimidex' in early breast cancer? New 100-month data from the ATAC Arimidex, Tamoxifen, Alone or in Combination ; trial, one of the world's largest and longest-running clinical trials in postmenopausal women with early breast cancer, found that compared with tamoxifen, Arimidex significantly: 1 o reduces the risk of all recurrences by 24% o improves disease free survival by 15% o reduces the risk of distant metastases recurrence elsewhere in the body ; by 16 and ashwagandha and Cheap arimidex online.
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A new drug called arimidex approved in july by health canada is will now bethe first-line treatment of choice in breast cancer.
Options granted in connection with the acquisition of OTL Pharma 3.8.1 Warrants granted to certain former shareholders in OTL Pharma At completion of the acquisition by the Company of OTL Pharma on 26 January 2004, the Company granted certain warrants to various former shareholders in OTL Pharma which are convertible into an aggregate of up to 750, 000 ordinary shares of 25p each in the share capital of the Company. The warrants were granted as part of the consideration for the acquisition by the Company of OTL Pharma. Those warrants are only convertible: i ; at the option of such warrantholder, if a Qualifying Issue as defined below ; occurs prior to the earlier of 25 July 2005 or the closure of an underwritten IPO; or ii ; automatically, on the earlier of 25 July 2005 or the closure of an underwritten IPO if a Qualifying Issue has occurred prior to that date, in each case in accordance with a formula set out in the instrument creating those warrants. For these purposes, as at 10 June 2005 being the latest practicable date prior to the date of this document ; , a Qualifying Issue was defined in the instrument creating those warrants as any issue of ordinary shares of 25p each in the capital of the Company for cash to investors at a subscription price per share that is less than 0.6667. As at 10 June 2005 being the latest practicable date prior to the date of this document ; , no such Qualifying Issue had been made. The instrument creating those warrants contains certain provisions that allow for the adjustment of the warrants in the event of certain reorganisations of the share capital of the Company. The Company intends to seek the agreement of the holders of those warrants to the adjustment of those warrants, conditional upon and with effect from immediately following the Capital Reorganisation but before Admission, such that those warrants will be convertible into an aggregate of up to 300, 000 Ordinary Shares and such that a Qualifying Issue will comprise an issue of Ordinary Shares at a subscription price per share that is less than 1.66675 per share. Accordingly, prospective investors should be aware that those warrants will convert on Admission into 299, 990 Ordinary Shares. Any shares in the capital of the Company, which are to be issued on conversion of those warrants, are to be issued by the Company to the holders of those warrants credited as fully-paid at par by the automatic capitalisation of an amount standing to the credit of the Company's share premium account or other available reserves. 3.8.2 OTL option agreements Pursuant to nine option agreements dated 26 January 2004 between the Company and various former holders of warrants over shares in OTL Pharma, the Company granted to those former holders of warrants over shares in OTL Pharma options to subscribe in cash for in aggregate 56, 704 ordinary shares of 25p each in the capital of the Company at a subscription price of 0.6667 per share in exchange for and conditional upon the transfer by each optionholder of those warrants to the Company. These options are exercisable at any time during the period from the date of signing of the option agreements until the earliest of certain events, including the tenth anniversary of the date of the relevant option agreement, the date of death of the optionholder and six weeks following the passing of a resolution for a members' voluntary winding up of the Company. The option agreements contain provisions that allow for adjustment of the outstanding options in the event of certain reorganisations of the share capital of the Company. The Company and the holders of these options have entered into agreements in terms of which they have agreed that the terms of these options will be adjusted to take into account the effect that the Capital Reorganisation will have on the share capital of the Company and duetact.
1 Australian Institute of Health and Welfare and Australasian Association of Cancer Registries. Cancer survival in Australia 2001. Part 1: National summary statistics. Canberra: Australian Institute of Health and Welfare, 2001. 2 Simpson ER. Sources of estrogen and their importance. J Steroid Biochem Molec Biol 2003; 86: 225-230. Lonning PE. Aromatase inhibition for breast cancer treatment. Acta Oncol 1996; 35 Suppl 5: S38-S43. 4 Buzdar AU, Robertson JF, Eiermann W, Nabholtz JM. An overview of the pharmacology and pharmacokinetics of the newer generation aromatase inhibitors anastrozole, letrozole, and exemestane. Cancer 2002; 95: 20062016. Bonneterre J, Buzdar A, Nabholtz JM, et al. Anastrozole is superior to tamoxifen as first-line therapy in hormone receptor positive advanced breast carcinoma. Cancer 2001; 92: 2247-2258. Mouridsen H, Gershanovich M, Sun Y, et al. Phase III study of letrozole versus tamoxifen as first-line therapy of advanced breast cancer in postmenopausal women: analysis of survival and update of efficacy from the International Letrozole Breast Cancer Group. J Clin Oncol 2003; 21: 2101-2109. Paridaens R, Dirix L, Lohrisch C, et al. Mature results of a randomized phase II multicenter study of exemestane versus tamoxifen as first-line hormone therapy for postmenopausal women with metastatic breast cancer. Ann Oncol 2003; 14: 1391-1398. Nabholtz JM, Buzdar A, Pollak M, et al. Anastrozole is superior to tamoxifen as first-line therapy for advanced breast cancer in postmenopausal women: results of a North American multicenter randomized trial. Arimidex Study Group. J Clin Oncol 2000; 18: 3758-3767. Tredway DR, Buraglio M, Hemsey G, Denton G. A phase I study of the pharmacokinetics, pharmacodynamics, and safety of single- and multiple-dose anastrozole in healthy, premenopausal female volunteers. Fertil Steril 2004; 82: 1587-1593. Effects of adjuvant tamoxifen and of cytotoxic therapy on mortality in early breast cancer. An overview of 61 randomized trials among 28 896 women. Early Breast Cancer Trialists' Collaborative Group. N Engl J Med 1988; 319: 1681-1692. Effects of chemotherapy and hormonal therapy for early breast cancer on recurrence and 15-year survival: an overview of the randomised trials Early Breast Cancer Trialists' Collaborative Group. Lancet 2005; 365: 1687-1717. Fisher B, Costantino JP, Wickerham DL, et al. Tamoxifen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study. J Nat Cancer Inst 1998; 90: 1371-1388. Goss PE, Ingle JN, Martino S, et al. A randomized trial of letrozole in postmenopausal women after five years of tamoxifen therapy for earlystage breast cancer. N Engl J Med 2003; 349 19 ; : 1793-1802. Epub 2003 Oct 9.
Arimidex is a hormonal treatment, not a cytotoxic chemotherapy treatment. It works by lowering the amount of the hormone estrogen in the body.
Secondary objectives: To compare surgery plus Arimidex with Arimidex alone PET ; in older women with ER + ve breast cancer in terms of: quality of life QoL ; , in order to determine whether Arimidex alone is superior to surgery plus Arimidex in terms of QoL; breast cancer specific survival, failure-free survival and local disease control, as secondary outcome measures to assess non-inferior anti-cancer efficacy of Arimidex alone; health economic assessment; Contralateral breast cancer rates, treatment related adverse events and skeletal related events will also be summarised. Further objectives: Development of a patient selection tool based on: Patient Characteristics To determine the patient characteristics which predict that the addition of surgery to Arimidex therapy will confer no benefit, comprehensive geriatric assessment based on the identification of factors associated with reduced life expectancy, including co-morbidity, functional status and cognitive function ; . Disease Characteristics To determine whether the tumour molecular profile predicts which women will respond well to PET with Arimidex in the long term. Translational studies: To determine the molecular changes associated with the development of secondary Arimidex therapy resistance.
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ILCU relating to the loss of access and lack of refund from the SPS on the disaffiliation of a credit union from ILCU. The plaintiff further contends that the defendants occupy a dominant position in the market for credit union representation services and seeks an order pursuant to s.14 7 ; of the Competition Act, 2002, requiring either that the dominant position be discontinued unless conditions specified in the order are complied with, or, alternatively, the adjustment of the dominant position in a manner and within a period specified in the order by a sale of assets or otherwise as the court may specify. ILCU is an unincorporated association which has its place of business at 33 41 Lower Mount Street in Dublin. The defendants are sued in their representative capacity as officers of the ILCU, having been nominated as defendants on behalf of ILCU to represent their members. Credit unions are individual autonomous savings and credit co-operatives established by individuals who have a "common bond". The most usual type of common bond is that of living or working within a particular community, with over 90% of all credit unions being based in a particular local community. The main objectives of credit unions are: The promotion of thrift, Helping members accumulate savings, Providing loans at reasonable rates of interest, and, The control of members' finances for their own benefit. As set out in the 2003 Annual Report of ILCU, the vision of credit unions is: "That ILCU, as an advocate of the credit union ethos of mutuality, volunteerism, self help, and a not-for-profit philosophy, will influence and inspire our movement and our society to achieve its social, economic and cultural objectives in a manner that respects the rights and dignity of everyone." The mission of ILCU is expressed as being: "To provide effective leadership for all credit unions on the island of Ireland, By fostering and maintaining unity and cooperation between credit unions, By developing a full range of top quality, safe and sound financial products and services, By recognising the dignity of credit unions and their members and their value to the community, and, By recognising the value and role of both credit union volunteers and staff to the movement and to society". In 1960, four credit unions came together for the purpose of trying to ensure that credit unions would conduct their affairs on the basis of a set of agreed operating principles and of presenting a united front to government and state agencies in relation to the legislative problems of credit unions. The unions who thus came together became known as the Irish League of Credit Unions. In 1966, the Credit Union Act was passed, by which time there were approximately 339 credit unions in ILCU. That Act provided that credit unions should have a set of operating rules in a form approved by the Registrar of Friendly Societies, who was to regulate credit unions under the Act. Pursuant to this requirement, the members of ILCU adopted a set of standard rules under which each member credit union would operate. These standard rules were approved by the Registrar in accordance and buy danazol.
Anagrelide Agrylin ; - for the treatment of essential thrombocythemia in patients who have failed or had intolerable side effects to treatment with hydroxyurea. Anastrozole Arimidex 1mg tablet ; - For the first-line treatment of post-menopausal patients with hormone receptor positive metastatic or locally advanced breast cancer. - For the treatment of adjuvant treatment upfront ; 1-5years ; of hormone receptor positive early stage breast cancer in post-menopausal patients who: - have a definite contraindication to tamoxifen OR - have demonstrated a severe intolerance to tamoxifen Anti-Tumor Necrosis Factor TNF ; Agents Etanercept, Infliximab, Adalimumab ; - for the treatment of Crohn's disease in adults, see Infliximab - for treatment of juvenile rheumatoid arthritis, see Etanercept - for the treatment of ankylosing spondilitis, see Adalimumab - for treatment of active psoriatic arthritis, see Etanercept, Adalimumab - for patients with a diagnosis of active rheumatoid arthritis RA ; : written request of a rheumatologist only have not responded or who have had intolerable toxicity to an adequate trial * of combination therapy of at least two traditional DMARDs * OR if combination therapy is not an option, an adequate trial of at least three traditional DMARDs in sequence as monotherapy AND -patients must have had an adequate trial * of leflunomide. Exceptions can be considered in cases where leflunomide is ineffective or contraindicated. therapy must include methotrexate * alone or in combination unless contraindicated or not tolerated coverage will be approved initially for 6 months. Can be reassessed for yearly coverage dependent on patient achieving an improvement in symptoms ACR ; of at least 20.
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Of Lagerstroemia speciosa L. has insulin-like glucose uptake-stimulatory and adipocyte differentiationinhibitory activities in 3T3-L1 cells. J Nutr. 2001 Sep; 131 9 ; : 2242-7. 5. Hayashi T, Maruyama H, Kasai R, Hattori K, Takasuga S, Hazeki O, Yamasaki K, Tanaka T. Ellagitannins from Lagerstroemia speciosa as activators of glucose transport in fat cells. Planta Med. 2002 Feb; 68 2 ; : 173 6. Hosoyama H, Sugimoto A, Suzuki Y, Sakane I, Kakuda T. [Isolation and quantitative analysis of the alpha-amylase inhibitor in Lagerstroemia speciosa L. ; Pers. Banaba ; ] Yakugaku Zasshi. 2003 Jul; 123 7 ; : 599-605. [Article in Japanese] 7. Kakuda T, Sakane I, Takihara T, Ozaki Y, Takeuchi H, Kuroyanagi M. Hypoglycemic effect of extracts from Lagerstroemia speciosa L. leaves in genetically diabetic KK-AY mice. Biosci Biotechnol Biochem. 1996 Feb; 60 2 ; : 204-8. 8. Judy WV, Hari SP, Stogsdill WW, Judy JS, Naguib YM, Passwater R. Antidiabetic activity of a standardized extract Glucosol ; from Lagerstroemia speciosa leaves in Type II diabetics. A dose-dependence study. J Ethnopharmacol. 2003 Jul; 87 1 ; : 115-7.
You can try Bellergal or Bellamine or Bellaspas, it's a belladonna, Cafergot-type preparation that I've found effective in some women. I guess you just need someone to work with you to try different recipes until something is found that works for you. LYNN M. SCHUCHTER, MD: The only thing I would say about the duration is this question of just doing two years of tamoxifen and then three years of an AI that the total hormonal therapy is five years. Kathy, do you want to talk about that? I don't know. You can skip it. KATHY S. ALBAIN, MD: No, because we don't know. See, the switching studies, that's what we did. But the caller several calls before her was talking about the.you know, do you do seven years or do you do just five years. And I tending toward making that aromatase inhibitor five years based on the trial of tamoxifen followed by letrozole, because the switching studies didn't have a third group that gave it for the full five years. But, see, that's without any data at all. So thank you, that's something we didn't cover. CALLER: I'm one of the ones who had extremely bad side effects from Arimidex. I had invasive ductal, one positive node, one cancer node, estrogen positive. I did dose density sic ; AC T and radiation and last year I tried the Arimidex because I had excellent bone density and I exercise a lot and all that good stuff. And I had just such debilitating joint ache and bone pain that I went off and it took about three months to feel normal, and I started tamoxifen in March and I'm doing quite well. My question, though, is I'm hoping that I can go back on an AI some point. But with all these AIs, because they cause joint pains and aches and bone density loss, is there any research that they're doing to look at trying to reduce that, to reduce those problems, those side effects? KATHY S. ALBAIN, MD: In terms of the bone aches and pains, I'm not familiar with anything that shows how to prevent it from starting. We've already talked about bone density and how to monitor that, and you're doing good things with the exercise. You sound just like a patient I have who I pleaded with to try a different one. And she's an avid golfer, and so the joint, the hand stuff was really affecting her. And.
In another. The study shows for the first time, that there is a potential biomechanical pathway associated with psychosocial stress resulting in increases in muscle coactivity & spine loading. Chapman-Smith. Chiropractic Report 1999; 13 2 ; : 1, 4, 5. poll commissioned by Canadian Chiropractic Assoc was done in November 1998 on a sample of 1, 515 adults, 1 month after a woman died of a stroke after a chiropractic treatment to assess the impact of the media blitz. Lack of knowledge of the educational qualifications of DCs was a much greater impediment to non-users to see a DC than risk of harm. 15% of respondents have been to a DC past 6 months, up from 11% in 1994 95 with a high in the Western provinces of 22%, 16% in Ontario & a low of 3% in Atlantic Canada. 53% were non-users: principal reasons I believe I have no need 75% ; & I don't see any benefits 16% ; . 90% agree that chiropractic treatment is good for certain people & 71% that chiropractic treatments are safe. 29% thought chiropractic was not safe: 22% said because treatment can be dangerous. Almost equally strong reasons were "DCs are not qualified" 20% ; "I have heard of bad experiences" 18% ; , "I don't believe in chiropractic 18% ; . The survey tested the impact of specific statements made to respondents & showed that the message most likely to improve opinions of DCs was "DCs are highly trained professionals" 37% ; . This had almost twice the power of any other message including `there are minimal risks associated with chiropractic treatment ." 23% ; . The main message DCs need to give the public relates to their education, qualifications & professional standing. Any communication campaign should have an educational focus "promoting positive info" rather than negative info risk rates. The goal should be "to enhance public opinion about the chiropractic profession .not necessarily to sell people on starting to use chiropractic.
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EContentplus 2007 Work Programme Implement solutions that make it easier for users both individuals and organisations, with special focus on SMEs ; to find and use existing digital educational content that matches their learning and skills development needs, for example as these are specified in competency profiles. Conditions: In addition to the common requirements for Targeted Projects, proposals should meet the following conditions: Digital content stakeholders, both public and private, as well as technology providers and pedagogical experts should be represented in a balanced way. Feedback mechanisms for end users, including teachers trainers and students learners as appropriate, should be provided on the usability of the content and on its quality, in terms of the effectiveness and efficiency of the learning process. The multilingual aspects of accessing and exploiting the content should be addressed in an efficient way appropriate for the educational use to be made of the underlying content. The multicultural aspects related to the use of the underlying content in different educational and learning cultures should be specifically addressed. Where appropriate, the use of open standards is recommended. Expected results: There will be a significant increase in the use and re-use of the underlying educational content across borders for learning in multiple languages and in different learning environments. Both professionally produced and user generated educational content will be made simultaneously accessible, cultural heritage and scientific content will be accessible for education, while mechanisms for matching learning needs with targeted material will be in place.
Ment trial that's ever been done. 9, 300 women around the world volunteered for this very, very important trial and the women had either - they were all post-menopausal because Arimidex therapy is only known to be effective for women who are post-menopausal. The women had node negative or node positive breast cancer and the vast majority of the women had estrogen receptor positive breast cancer. And the women were randomized. They either got chemotherapy or didn't. It could go either way there and they were randomized to Arimidex, which is a new pill. It's an anti-estrogen that works differently than Tamoxifen. Tamoxifen has been around 30 years. Tamoxifen binds directly to the estrogen receptor and prevents estrogen from stimulating breast cancer cells to grow. Arimidex works differently in postmenopausal women. It prevents the ovary, the muscles, and the fat cells from making estrogen. So it prevents the body from making estrogen in the first place. And so, Arimidex - one-third of the women got Arimidex, one-third got Tamoxifen, and onethird got the combination of Tamoxifen and Arimidex. And the first data from the ATAC trial were presented at the San Antonio breast cancer conference in 2001 and that was a three-year update. That was the first time it was presented - the data - and the women had an average of three years on the study. And what was shown there is: first, there was no benefit of the combination of Arimidex and Tamoxifen compared to Tamoxifen alone. And so, what's happened subsequently is that the women who were getting the combination were told they were getting the combination and then their doctors were able to choose whether to continue that woman on Arimidex or Tamoxifen. And so that's what happened in that clinical trial with the three-year follow up. And, in fact, that was no different in the four-year follow up this year. So the real comparison, then, came down to looking at Arimidex versus Tamoxifen. And at three years of follow up when it was first presented at 2001, there was a two-percentage point absolute benefit in favor of Arimidex when one looked at recurrence of the breast cancer - of a woman's breast cancer in her breast, or in the rest of her body, or the development of a new breast cancer in her other breast. So it was a two-percentage point difference in terms of recurrence; no difference in survival because it was way too early. The.
31 ; Smith CL, Nawaz Z, O'Malley BW. Coactivator and corepressor regulation of the agonist antagonist activity of the mixed antiestrogen, 4-hydroxytamoxifen. Mol Endocrinol 1997; 11: 657 ; Takimoto GS, Graham JD, Jackson TA, Tung L, Powell RL, Horwitz LD, et al. Tamoxifen resistant breast cancer: coregulators determine the direction of transcription by antagonist-occupied steroid receptors. J Steroid Biochem Mol Biol 1999; 69: 4550. ; Dombernowsky P, Smith I, Falkson G, Leonard R, Panasci L, Bellmunt J, et al. Letrozole, a new oral aromatase inhibitor for advanced breast cancer: double-blind randomized trial showing a dose effect and improved efficacy and tolerability compared with megestrol acetate. J Clin Oncol 1998; 16: 453 ; Gershanovich M, Chaudri HA, Campos D, Lurie H, Bonaventura A, Jeffrey M, et al. Letrozole, a new oral aromatase inhibitor: randomised trial comparing 2.5 mg daily, 0.5 mg daily and aminoglutethimide in postmenopausal women with advanced breast cancer. Letrozole International Trial Group AR BC3 ; . Ann Oncol 1998; 9: 639 ; Mouridsen H, Gershanovich M, Sun Y, Perez-Carrion R, Boni C, Monnier A, et al. Phase III study of letrozole versus tamoxifen as first-line therapy of advanced breast cancer in postmenopausal women: analysis of survival and update of efficacy from the International Letrozole Breast Cancer Group. J Clin Oncol 2003; 21: 21019. ; Buzdar AU, Jonat W, Howell A, Jones SE, Blomqvist CP, Vogel CL, et al. Anastrozole versus megestrol acetate in the treatment of postmenopausal women with advanced breast carcinoma: results of a survival update from two mature phase III trials. Arimidex Study Group. Cancer 1998; 83: 1142 ; Kaufmann M, Bajetta E, Dirix LY, Fein LE, Jones SE, Zilembo N, et al. Exemestane is superior to megestrol acetate after tamoxifen failure in postmenopausal women with advanced breast cancer: results of a phase III randomized double-blind trial. The Exemestane Study Group. J Clin Oncol 2000; 18: 1399 ; Goss PE, Ingle JN, Martino S, Robert NJ, Muss HB, Piccart MJ, et al. A randomized trial of letrozole in postmenopausal women after five years of tamoxifen therapy for early-stage breast cancer. N Engl J Med 2003; 349: 1793 ; Jeng MH, Shupnik MA, Bender TP, Westin EH, Bandyopadhyay D, Kumar R, et al. Estrogen receptor expression and function in long-term estrogendeprived human breast cancer cells. Endocrinology 1998; 139: 4164 ; Masamura S, Santner SJ, Heitjan DF, Santen RJ. Estrogen deprivation causes estradiol hypersensitivity in human breast cancer cells. J Clin Endocrinol Metab 1995; 80: 2918.
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