| Referred to as a "Non-spawning Fish Screening Assay" and is based upon the measurement of three core endpoints, namely vitellogenin, gonado-somatic index GSI ; and gonad histopathology [2]. For example, Panter et al. [33] reported a 21d adult fathead minnow assay measuring VTG and GSI response to estrogens. More recent work in Europe has extended this approach to juvenile fathead minnows using a variety of weak and potent antiestrogens [9]. Similarly, the Japanese Ministry of Environment [34] has successfully used a 14 to 21-day medaka screening assay to comprehensively detect benzophenone, di-cyclohexyl phthalate, di-ethyl phthalate, octylphenol, and triphenyltin chloride. Moreover, this approach has been successfully adopted for the rapid detection of xenoestrogens in sheepshead minnows [16] and zebrafish [13, 14]. In addition to inducing VTG titres, xenoestrogen exposure has also been shown to reduce gonadosomatic index and cause histological changes in gonads of zebrafish after between 6 to 24 days [14]. In summary, available data indicate that the nonspawning fish screening test can be successfully in OECD fish species for the rapid detection within 1421 days ; of a range of EASs. Other protocols that may have a future role in chemical testing programs are described below. FISH DEVELOPMENT TEST EXTENDED ELSs TEST ; It is now well established from aquaculture that fish early life-stages ELSs ; are sensitive to EASs. This fact, together with a reliance in regulatory ecotoxicology on the fish ELSs test for chronic hazard assessments [35] has led to the concept of a new "Fish Development Test" which can be seen as an extended ELSs test [36]. Depending on the suspected mode of action of an EAS based on information gained in mammalian and fish screening assays ; , the assessment of developmental affects caused by EASs should include survival, growth, development, gonad histology, and VTG up to 90100 days posthatch. Demonstrations of aspects of this test concept have recently been reviewed [36]. Further details of the approach are illustrated for medaka. Medaka development test As medaka is a gonochoristic species showing no hermaphroditism under natural conditions ; a medaka development test could effectively address EAS-induced sex-reversal, one of the main endpoints of endocrine-disrupting effects. For example, the medaka sex-reversal assay is based on the d-rR and S-rR strains see above ; . In the sex-reversal test, the sex-linked colors are unchanged by exposure to EASs but sex-reversal is identified by the gonad histology as well as the secondary sexual characteristics dorsal and anal fins ; . Fish are exposed to a chemical during their susceptible periods from the prelarva just after hatching to 28 days post-hatch and then reared for an additional 14 days in clean dilution water until their functional sexes become detectable. At the age of 42 days at 24 C ; , fish with a total length more than 20 mm are fixed and examined for secondary sexual characteristics on the dorsal fin maximum length, and cleft depth between the last ray and preceding one ; and anal fin [maximum length, length of second ray from the last, and appearance of small anal papillary processes app ; on the posterior region]. Thereafter, serial cross sections of gonads of the fish are made and observed microscopically. The medaka sex-reversal test has been applied to a variety of chemicals, including 17-ethinylestradiol EE2 ; , 17-estradiol E2 ; , diethylstilbestrol DES ; 4-t-pentylphenol 4tPP ; , methyltestosterone MT ; , and flutamide Flu ; . The existence of a secondary sexual characteristic of males, small papillary processes on the anal fin, was confirmed in almost all genotypic males but not in control females Fig. 1 ; . In contrast, this character increased in genotypic females exposed to MT at 0.1 g l. No change was observed in either males or females exposed to Flu even at the highest concentration 1000 g l ; . The gonads of male and female control fish naturally differentiated to testis or ovary, respectively Fig. 2 ; . Gonads of genotypic males exposed to EE2, DES, 4tPP, and E2 differentiated into ovaries with LOECs of 0.032 g l, 0.032 g l, 10 g l, and 0.1 g l, respectively. On the con 2003 IUPAC, Pure and Applied Chemistry 75, 23432353.
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Acta Physiologica Sinica, April 25, 2004, 56 ; : 147-152 Lowry OH, Rosebrough HJ, Farr AL. Protein measurement with Folin-Phenol reagent. J Biol Chem 1951; 193: 265-275. Sambrook J, Fritsch EF, Maniatis T, eds. Immunoassay of Expressed Protein, Molecular Cloning: A Laboratory Manual. 2nd ed. Cold Spring Harbor Laboratory Press, 1989: 880. Shen WH, Zhang CY, Zhang GY. Modulation of IB kinase autophosphorylation and activity following brain ischemia. Acta Pharmacol Sin 2003; 24: 311-315. MacManus JP, Linnik MD. Gene expression induced by cerebral ischemia: an apoptotic perspective. J Cereb Blood Flow Metab 1997; 17: 815-832. Merry DE, Korsmeyer SJ. Bcl-2 gene family in the nervous system. Annu Rev Neurosci 1997; 20: 245-267. Gillardon F, Lenz C, Waschke KF, Krajewski S, Reed JC, Zimmermann M, Kuschinsky W. Altered expression of Bcl-2, Bcl-X, Bax, and c-Fos colocalizes with DNA fragmentation and ischemic cell damage following middle cerebral artery occlusion in rats. Brain Res Mol Brain Res 1996; 40: 254-260. Urabe T, Hattori N, Yoshikawa W, Yoshino H, Uchida K, Mizuno Y. Colocalization of Bcl-2 and 4-hydroxynonenal modified proteins in microglial cells and neurons of rat brain following transient focal ischemia. Neurosci Lett 1998; 247: 159-162. Choi DW. Glutamate neurotoxicity and diseases of the nervous system. Neuron 1988; 1: 623-634. Choi DW. Glutamate receptors and the induction of excitotoxic neuronal death. Prog Brain Res 1994; 100: 47-51. Budd SL, Tenneti L, Lishnak T, Lipton SA. Mitochondrial and extramitochondrial apoptotic signaling pathways in cerebrocortical neurons. Proc Natl Acad Sci 2000; 97: 6161-6166. Marshall KA, Daniel SE, Cairns N, Jenner P, Halliwell B. Upregulation of the anti-apoptotic protein Bcl-2 may be an early event in neurodegeneration: studies on Parkinson s and incidental Lewy body disease. Biochem Biophys Res Commun 1997; 240: 84-87.
INTRODUCTION Androgen receptor AR ; function is required for male sex development in the fetus, virilization at puberty, and maintenance of reproductive function in the adult. Interruption of these processes by pharmacological androgen antagonists or environmental endocrine disruptors can cause incomplete masculinization of the fetus or possibly reduced male fertility later in life 1, 2 ; . Overstimulation of the prostate by androgen agonists may promote prostate cancer 3 ; . Experimental approaches to identify and distinguish AR agonists from antagonists would aid in the classification of environmental and pharmaceutical chemicals since ligandbinding affinity alone does not necessarily reflect biological potency, and transient transcriptional assays can be hampered by the complexity of the systems. Previous studies from this laboratory identified an AR NH2-terminal and carboxyl-terminal N C ; interaction that requires high-affinity androgen binding 4 ; . The androgen-induced N C interaction is inhibited by the androgen antagonist hydroxyflutamide. These results raised the possibility that an N C interaction is and raloxifene.
ESTROGEL .55 estrogens, conjugated .55 estrogens, conjugated synthetic a .56 estrogens, esterified .56 estropipate .54 ESTROSTEP FE .56 eszopiclone.68 etanercept .60 etanercept 25 mg .60 etanercept 50 mg .60 ethacrynate sodium .36 ethacrynic acid .36 ethambutol hcl .22 ETHEDENT .71 ETHEXDERM BPW-10 .45 ETHEXDERM BPW-5 .45 ethinyl estradiol & etonogestrel .56 ethinyl estradiol & norelgestromin .56 ethinyl estradiol & norethindrone .54, 56 ethinyl estradiol & norethindrone acetate .56 ethinyl estradiol & norgestimate .56 ethinyl estradiol-ferrous fumarate-norethindrone acetate .56 ethionamide .22 ETHMOZINE .34 ethosuximide .16, 17 ethotoin .18 ETIDRONATE DISODIUM.52 etidronate disodium.52 etodolac.10 etodolac cr .10 EULEXIN * See flutamide .57 EURAX .45 EVISTA .56 EXELDERM .21 EXELON.18 EXELON SOLN .18 exemestane .23 exenatide .29 EXJADE .33 EXUBERA .30 EXUBERA KIT .30 ezetimibe.37 ezetimibe and simvastatin .37.
Geriatric Use: Clinical trials of LIALDA did not include sufficient numbers of patients aged 65 and over to determine whether they respond differently from younger patients. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concurrent disease or other drug therapy. ADVERSE REACTIONS LIALDA tablets have been evaluated in 655 ulcerative colitis patients in controlled and open-label trials. In two 8-week placebo-controlled clinical trials involving 535 ulcerative colitis patients, 356 received 2.4g day or 4.8g day LIALDA tablets and 179 received placebo. More treatment emergent adverse events occurred in the placebo group 119 ; than in each of the LIALDA treatment groups 109 in 2.4g day, 92 in 4.8g day ; . A lower percentage of LIALDA patients discontinued therapy due to adverse events compared to placebo 2.2% vs 7.3% ; . The most frequent adverse event leading to discontinuation from LIALDA therapy was exacerbation of ulcerative colitis 0.8% ; . The majority of adverse events in the double blind, placebo-controlled trials were mild or moderate in severity. The percentage of patients with severe adverse events was higher in the placebo group 6.1% in placebo; 1.1% in 2.4g day; 2.2% in 4.8g day ; . The most common severe adverse events were gastrointestinal disorders which were mainly symptoms associated with ulcerative colitis. Pancreatitis occurred in less than 1% of patients during clinical trials and resulted in discontinuation of therapy with LIALDA in patients experiencing this event. Overall, the percentage of patients who experienced any adverse event was similar across treatment groups. Treatment related adverse events occurring in LIALDA or placebo groups at a frequency of at least 1% in two Phase 3, 8-week, double blind, placebo-controlled trials are listed in Table 3. The most common treatment related adverse events with LIALDA 2.4g day and 4.8g day were headache 5.6% and 3.4%, respectively ; and flatulence 4% and 2.8%, respectively ; . Table 3. Treatment Related Adverse Events in Two Phase 3 Trials Experienced by at Least 1% of the LIALDA Group and at a Rate Greater than Placebo and efavirenz, because what is flutamide.
Haematuria was reported in 12% of patients receiving `Casodex' plus LHRHa and 6% of patients receiving flutamide plus LHRHa, p 0.007. However, the majority of cases 90% ; were mild to moderate in intensity, were not related to treatment, and did not lead to treatment withdrawal.56.
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Introduction: Frontal traffic collisions produce unique vehicle deformation patterns that depend on the object that is struck. Oftentimes the investigating engineer can quickly determine what category of object was impacted based on the observed residual collision damage, because collisions with other vehicles, concrete walls, or trees will produce unique crush patterns. Impacts with narrow objects such as trees or utility poles create knife-like deformation patterns. Narrow object impacts often create deformation that penetrates deeper into the vehicle's structure when compared to an impact with an object that distributes collision forces over a greater width of the vehicle at the same speed. Induced damage is created when the vehicle wraps around the narrow object, and pulls the lateral components at the left and right inward. The deformation pattern of two vehicles impacting trees will be presented. A damage energy analysis was used to determine the impact speed from the measured longitudinal collision damage and other scene information. The extent of vehicle damage and the subsequent structural compromises will be explored. The vehicle models in these two cases are the same and the vehicle weights are similar, but what is different is the location of the tree impact relative to the vehicle centerline. In the first case, the tree impact location is inches to the left of the vehicle centerline, whereas in the second case, the tree impact location is at the extreme left end of the bumper. Collision Overview: The first case concerns a 1988 Nissan Maxima 4-door sedan Nissan #1 ; , containing two male occupants, a driver and right front passenger, traveling at approximately 55 to 65 mph. After crossing a broken double-yellow centerline while attempting to pass slower traffic ahead, the Maxima was struck on the right by another vehicle also attempting to pass slower traffic. The Maxima's heading was forcefully redirected to the left, and it subsequently entered the left-hand shoulder. Differential friction between the inadequately packed, loose shoulder material and the asphalt covered road created an unfortunate situation for which the driver could not recover. The vehicle entered the shoulder and then re-entered the roadway several times until it ultimately struck a 12inch diameter tree head-on located approximately 17 feet measured perpendicular from the road. The second case concerns a 1987 Nissan Maxima 4-door sedan Nissan #2 ; , containing only a female driver, traveling in the #1 lane at approximately 45 mph. A vehicle in lane #2 suddenly veered left into lane #1, sideswiping the right side of the Nissan. The impact caused the Nissan driver to lose control, suddenly steer to the left and rise over the 5 inch curb of the center median, and then strike a 14-inch diameter tree head-on. Due to the offset nature of the frontal impact with the tree, the Nissan subsequently yawed counter-clockwise, and then rolled over passenger side leading, coming to rest on its wheels approximately 48 feet beyond the tree. Energy Analysis: Both collision vehicles were inspected and the residual collision damage was measured across the front bumper using a suitable reference coordinate system. An exemplar vehicle was inspected and its front bumper was similarly profiled. Scale drawings were used to quantify the residual collision damage. Vehicle crush stiffness characteristics A and B values ; were calculated from available government-sponsored barrier crash tests. The Campbell model, assuming a linear relationship between energy and crush, was used to calculate the vehicle's pre-impact speed. Nissan #1, including the two occupants, weighed approximately 3570 lb. It sustained 20 inches of average residual crush. The corresponding crush energy was approximately 1.941x10 6 in-lb. After impact, Nissan #1 came to rest very close to the tree. That is, Nissan #1 had very little postimpact energy. Its pre-impact speed was determined to be approximately 37 mph. By comparison, Nissan #2, including the driver, weighed approximately 3330 lb. It sustained 20.7 inches of average residual crush. The corresponding crush energy was approximately 1.804x10 6 in-lb. After impact, Nissan #2 rotated away from the tree, and the vehicle subsequently rolled over. After calculating the post-impact energy, the preimpact speed was determined to be approximately 44 mph and vaseretic.
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36. Iversen P, Rasmussen F, Klarskov P, Christensen IJ. Long-term results of Danish Prostatic Group trial 86; goserelin acetate plus flutamide versus orchidectomy in advanced prostate cancer. Cancer Suppl 1993; 72: 3851-4. Fourcade RO, Colombel P, Mangin M. Zoladex plus flutamide versus zoladex plus placebo in advanced prostatic carcinoma: extended follow-up of the French multicentre study. In: Murphy G, Khoury S, Chatelain C, Denis L eds. Proceedings of the 3rd International Symposium on Recent Advances in Urological Cancer: Diagnosis and Treatment, June 1992, Paris, France, 1993; 102-6. 38. Zalcberg JR, Raghavan D, Marshall V, Thompson PJ. Bilateral orchidectomy and flutamide versus orchidectomy alone in newly diagnosed patients with metastatic carcinoma of the prostate: an Australian multicentre trial. Br J Urol 1996; 77: 865-9. Delaere KP, Boccon-Gibod L, Corrado F. Randomized, double-blind, parallel group study of flutamide and orchidectomy versus placebo and orchidectomy in men with D2 adenocarcinoma of the prostate [Abstract]. Proc ECCO-4 1987; 68. 40. Boccardo F, Pace M, Rubagotti A, Guarneri D, Decensi A, Oneto F et al. Goserelin acetate with or without flutamide in the treatment of patients with locally advanced or metastatic prostate cancer: the Italian Prostatic Cancer Project PONCAP ; Study Group. Eur J Cancer 1993; 29A: 1088-93. Ferrari P, Castagnetti G, Ferrari G, Polastri CA, Baisi B, Dotti A. Combination treatment versus LHRH alone in advanced prostatic cancer. Urol Int 1996; 56: 13-7. Eisenberger MA, Blumenstein BA, Crawford ED, Miller G, McLeod DG, Loehrer PJ. Bilateral orchiectomy with or without flutamide for metastatic prostate cancer NCI INT-0105 SWOG-ECOG ; . N Engl J Med 1998; 339: 1036-42. Bono AV, Di Silverio F, Robustelli della Cuna G, Benvenuti C, Brausi M, Ferrari P et al. Complete androgen blockade versus chemical castration in advanced prostatic cancer: analysis of an Italian multicentre study. Italian Leuprorelin Group. Urol Int 1998; 60: 18-24. Robinson MR, Smith PH, Richards B, Newling D, de Pauw M, Sylvester R. The final analysis of the EORTC Genito-Urinary Tract Center Co-operative Group phase III clinical trial protocol 30805 ; comparing orchidectomy, orchidectomy plus cyproterone acetate and low dose stilboestrol in the management of metastatic carcinoma of the prostate. Eur Urol 1995; 28: 273-83. Di Silverio F, Serio M, D'Eramo G, Sciarra F. Zoladex vs. zoladex plus cyproterone acetate in the treatment of advanced prostatic cancer: A multicenter Italian study. Eur Urol 1990; 18: 54-61. de Voogt HJ, Studer U, Schroder FH, Klijn JG, de Pauw M, Sylvester R. Maximum androgen blockade using LHRH agonist buserelin in combination with short-term twoweeks ; or long-term continuous ; cyproterone acetate is not superior to standard androgen deprivation in the treatment of advanced prostate cancer: final analysis of EORTC GU Group Trial 30843. Eur Urol 1998; 33: 152-8. Jorgensen T, Tveter KJ, Jorgensen LH. Total androgen suppression: experience from the Scandinavian Prostatic Cancer Group Study No.2. Eur Urol 1993; 24: 466-70. Thorpe SC, Azmatullah S, Fellows GJ, Gingell JC, O'Boyle PJ. A prospective, randomised study to compare goserelin acetate Zoladex ; versus cyproterone acetate Cyprostat ; versus a combination of the two in the treatment of metastatic prostatic carcinoma. Eur Urol 1996; 29: 46-54. Thei M, Wirth M, Tunn U. Triptorelin-cyproteronacetate versus Triptorelin-Placebo: Multizentrische Phase III-Studie an 222 Patienten met fortgeshrittenem Prostata-Karzinom [Abstract]. Urologe A 1996; S41 and ethambutol.
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Summation of substances causing orientation. Because of the extremely low concentrations in which they are active it is not possible to test the substances shown in Tables i and 2 for summation. This could, however, be studied with substances whose activity is approximately 2, i.e. those which also cause biting. Only two substances were tested, viz. glucose and sucrose. With fed wireworms no orientation is caused by 0-5 % solutions of glucose or 0-126% solutions of sucrose, while o-8% solutions of glucose and 0-25% solutions of sucrose are active. The activities of these sugars are therefore: glucose 2-1 and sucrose 2-6. Mixed solutions containing 0-5% glucose and 0-126% sucrose are active, showing that summation has occurred Fig. 1 and myambutol!
I. Background. Beginning in late 2004, the parties in this Multi-District Litigation "MDL" ; provided each other with designations of their "core experts" that is, experts who will offer "generally applicable" testimony in more than one of the MDL constituent cases.1 Plaintiffs designated 17 core experts, and defendants designated 30 core experts; the areas of expertise include neurology, neuro-pathology, neuro-psychology, neuro-radiology, epidemiology, bio-statistics, industrial hygiene, industrial engineering, chemistry, materials science, warnings, corporate ethics, military specification and procurement procedures, economics, government lobbying, and ancient corporate documents. Following deposition of these experts, the parties filed numerous motions invoking Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 1993 ; , arguing that some or all of the proposed testimony of some of these experts should be excluded. In addition to reviewing these briefs and the many attached exhibits, 2 the Court held a Daubert hearing over a period of several days. At this hearing, the parties presented argument and expert testimony, and questions were put to both the attorneys and the experts by the undersigned, by the MDL Special Master David R. Cohen ; , and by the Special Master appointed to oversee the related state court litigation known as California Judicial Council Coordination, for example, flutamid3 prostate.
The doctors conducting the tests must not be members of the transplant team. The `Criteria for Diagnosis of Brain Stem Death' form should be completed and signed by both doctors and filed in the patients medical records see Appendix A and etoposide.
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Figure 5. Diagram illustrating an extension of Solomon and Corbit's 1974 ; opponent-process model of motivation to outline the conceptual framework of the allostatic hypothesis. Both panels represent the affective response to the presentation of a drug. Top ; This diagram represents the initial experience of a drug with no prior drug history, and the a-process represents a positive hedonic or positive mood state, and the b-process represents the negative hedonic of negative mood state. The affective stimulus state ; has been argued to be a sum of both an a-process and a b-process. An individual whom experiences a positive hedonic mood state from a drug of abuse with sufficient time between re-administering the drug is hypothesized to retain the a-process. In other words, an appropriate counteradaptive opponent-process b-process ; that balances the activational process a-process ; does not lead to an allostatic state. Bottom ; The changes in the affective stimulus state ; in an individual with repeated frequent drug use that may represent a transition to an allostatic state in the brain reward systems and, by extrapolation, a transition to addiction. Note that the apparent b-process never returns to the original homeostatic level before drug-taking is reinitiated, thus creating a greater and greater allostatic state in the brain reward system. In other words, the counteradaptive opponent-process b-process ; does not balance the activational process a-process ; but in fact shows a residual hysteresis. While these changes are exaggerated and condensed over time in the present conceptualization, the hypothesis here is that even during post-detoxification, a period of "protracted abstinence, " the reward system is still bearing allostatic changes. In the nondependent state, reward experiences are normal, and the brain stress systems are not greatly engaged. During the transition to the state known as addiction, the brain reward system is in a major underactivated state while the brain stress system is highly activated. Small arrows refer to increased or decreased functional activity of the neurotransmitters. DA, dopamine; CRF, corticotropin-releasing factor; GABA, gamma-aminobutyric acid. The following definitions apply: allostasis, the process of achieving stability through change; allostatic state, a state of chronic deviation of the regulatory system from its normal homeostatic ; operating level; allostatic load, the cost to the brain and body of the deviation, accumulating over time, and reflecting in many cases pathological states and accumulation of damage [Modified with permission from Koob & Le Moal 11 ; ].
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Citation 33, 3639 ; . Moreover, depressed adrenal function is not uncommon in the clinical arena, and the incidence of adrenal insufficiency increases in critically ill patients in the surgical intensive care unit 2, 4, 6, ; . Our recent findings also indicate that depressed adrenal function occurs early following trauma and severe hemorrhage in male animals 34 ; . Because depressed adrenal function is usually associated with cardiovascular dysfunction and depressed function in other organs after various stresses 10, 13 ; , including hemorrhage 12, 13 ; , it is important to investigate potential therapeutic approaches for maintaining adrenal function following trauma and hemorrhage. Recent studies have examined the role of sex hormones in the pathophysiology of trauma and severe hemorrhage 1, 4143 ; . It has been demonstrated that female animals show a normal or even enhanced immune response after trauma and hemorrhage, whereas males exhibit a depressed immune response 42 ; . Furthermore, since gonadectomy before the induction of trauma and hemorrhage in male mice prevents the occurrence of the immune depression 43 ; , this suggests that male sex hormones may play an important role in the regulation of posttraumatic immune responses. Moreover, flutamide, a nonsteroidal testosterone receptor antagonist, has been shown to restore the depressed immune function in males after hemorrhage 1, 41 ; . In regard to organ functions, administration of fltuamide following trauma and hemorrhage has been shown to improve the depressed cardiac and hepatic functions in male rats 28 ; . However, it remains unknown whether this agent has any salutary effects on the depressed adrenal function in males under such conditions. Therefore, the aim of this study was to determine whether testosterone receptor blockade with flutamide following trauma and severe hemorrhagic shock attenuates depressed adrenal function under those conditions in male animals.
Europeans [52], who constitute the majority of patients in the flutamide studies. It has been reported that 98% of 54 patients who could not tolerate flutamide due to diarrhea did not withdraw because of diarrhea from subsequent therapy with bicalutamide [53]. Hepatic Toxicity Laboratory Test Abnormalities Abnormal liver function tests, in particular elevated transaminases, have been reported with all three nonsteroidal antiandrogens. While some of the abnormal results can undoubtedly be attributed to concomitant medications or underlying disease, an association with the antiandrogens cannot always be ruled out. Incidences of abnormal liver function test results have been variously reported from 2%-33% in nilutamide groups [13, 32, 33, 45] and from 4%-62% in flutamide groups [5, 7, 9, 11, in trials of monotherapy and CAB. In a study of LHRH-A plus flutamide or placebo, elevated aminotransferases were significantly more common in the flutamide group than in the placebo group 12% versus 3%; p 0.01 ; [9]. Furthermore, the transcript of the proceedings of the 1988 FDA Advisory Committee Meeting [50] included discussion of data from the large study comparing flutamide plus LHRH-A with LHRH-A alone [4]. When adverse events irrespective of causality were considered, a marginal treatment effect was detected with regard to hepatic adverse events in the flutamide group compared with the placebo group 16% versus 10%; p 0.05 ; . In the double-blind, comparative study of flutamide plus LHRH-A versus bicalutamide plus LHRH-A, elevated transaminases occurred in slightly more patients in the flutamide group than in the bicalutamide group 10% versus 6%; p 0.07 ; . This increased incidence was also seen for patients with greatly elevated 5 normal ; transaminase values 2% versus 0.5% ; [22, 46]. Clinical Hepatotoxicity Clinical hepatotoxicity has also been associated with all three nonsteroidal antiandrogens, but there are differences among the three drugs with respect to the nature and severity of the reported conditions. While hepatic failure has been seen with both flutamide and nilutamide, it has not been attributed to the use of bicalutamide in studies of monotherapy or CAB involving 3, 717 men [46]. Five patients exhibited jaundice in which bicalutamide-induced hepatotoxicity could not be ruled out, and jaundice of unknown origin ; was thought to contribute to the death of one patient with prostate cancer and chronic renal failure [46]. One case of acute, reversible hepatitis and one case of fatal, fulminant hepatitis have been described in the literature and femara.
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497. MOLECULAR MODELING OF ASPARAGINE SYNTHETASE. Robert Humkey, Yun Ding, and Nigel G.J. Richards, Department of Chemistry, University of Florida, Box 117200, Gainesville, FL 32611-7200, humkey qtp.ufl The enzyme asparagine synthetase AS ; catalyzes the biochemical conversion of aspartate to asparagine. A direct correlation between the development of drug-resistance in leukemia and the over-expression of AS has recently been observed. This connection has led to the belief that an inhibitor of AS would be able to reverse the effects of drug resistance in leukemia cells. A molecular model of E. coli asparagine synthetase-B AS-B ; will be presented as the first complete structural insight into the critical active sites of this enzyme. The model is being used to examine the different effects of the binding of structurally analogous inhibitors and non-inhibitors on AS-B, as well as identifying the specific active site interactions that can be used to facilitate inhibitor binding. 498. NOVEL INHIBITORS OF CARBONYL REDUCTASE. Berea Williams, Corianton L. Larson, Andrew Slupe, Kristofor Olson, Sanela Begic, Laura Lee, and Henry A. Charlier Jr., Department of Chemistry, Boise State University, 1910 University Drive, Boise, ID 83725-1520, willbere2000 yahoo Anthracyclines are effective antineoplasticagents, but are known to cause a potentially lethal chronic cardiomyopathy, which severely limits their use. Anthracycline cardiotoxicity has been linked to the formation of a metabolite catalyzed by carbonyl reductase CR ; . Since the metabolite does not possess the antineoplastic properties of its parent anthracycline, the action of CR may also contribute to drug resistance. In an effort to prevent the CR derived formation of the cardiotoxic metabolite, CR inhibitor candidates were tested. Of the compounds that were tested, two were found to be noncompetitive inhibitors against both coenzyme and carbonyl substrates, with KI values in the low micromolar range. The inhibition patterns suggest that the inhibitors bind to multiple enzyme forms. Intrinsic protein fluorescence quenching studies demonstrated that the inhibitors bind to at least the free enzyme and to an enzyme product binary complex with Kd values similar to the KI values. Supported by NIH P20RR16454, NIH R15CA102119-01. 499. INVESTIGATION OF POLYAMINE ANALOGS ON THE GROWTH OF MCF-7 BREAST CANCER CELL LINES. Michelle Piel, Kristina Thornburg, Christopher Higgins, Francis Charles Mayville Jr., and Peter Leonard, Natural Science Department, DeSales University, 2755 Station Avenue, Center Valley, PA 18034, Fax: 610-282-0525, fcm0 desales , fcm0 desales In this study, we are synthesizing new polyamine analogs using 1, 4-diaminobutane putrescine ; as the template. The new polyamine derivatives will contain two, three, or four carbon primers at the each amino end of the putrescine. It has been previously determined that the polyamine systems can bind to the minor grooves of DNA molecules and inhibit cell growth. In other previous work, the inhibition of cell growth has been studied using several synthesized polyamine derivatives, and it was found that these artificial systems had more inhibition ability then natural polyamines. In our study, the new polyamine systems will be compared with current polyamine analogs to determine their efficacy for inhibition of cell growth in MCF-7 breast cancer cell lines. The methods of analysis will include HPLC analysis of nuclear DNA and gross cell counting.
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Since a steady state is achieved. In a steady-state process, line graphs can be used to depict temporal sequences, although animals were not sacrificed serially. We suggest that their primary groups with one suitable ber for visual of any of cells use be to compare another. Finally, portrayal one type present Hx and Hx-flutamide line graphs are more The within greatest the numseminif.
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Flutamide-treated males fed the Phyto-600 diet made significantly fewer errors than flutamide-treated males fed the Phyto-free diet. In other words, feminized males via the flutamide treatments ; fed the Phyto-600 diet outperformed feminized males fed the phytoestrogenfree diet. This result is similar to intact females on the Phyto-600 diet outperforming intact females on the Phyto-free diet, as observed in our companion paper.
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This project aimed at strengthening scientific approach concerning the effects on male fertility of exposure to environmental factors such as endocrine disrupters. The objective was to use DNA microarray approach to improve the current approach for assessing the endocrine androgen ; disrupting effects of chemicals such as flutamide on testicular development and function. Specific aims were to: i ; identify among thousands of testicular genes those affected by antiandrogenic flutamide and finasteride ; disruption using the DNA microarray approach; ii ; understand the specificity and the function s ; of the proteins encoded by these genes in the activity of testicular germ, Sertoli and Leydig cells. As this is a genomic approach to identify the transcripts, the levels of which are affected in the different testicular major cell types, the doses of flutamide were chosen in order to avoid or minimise germ cell loss that may confound the interpretation of effects of flutamide on testicular germ cell ; gene expression. For these reasons, the doses of the antiandrogen selected were 0.4, 2 and 10 mg kg day. The project was subdivided in 5 work packages WP ; that were conducted in parallel as follows: WP01 was devoted to the project coordination WP02 corresponded to the production of DNA microarrays, mainly from rat testis cDNA libraries. By using these DNA microarrays and the testis transcripts obtained from male rats treated during their foetal life with antiandrogens at different concentrations WP03 ; , the.
Professor Jack Satsangi, Gastrointestinal Unit, Molecular Medicine Centre, University of Edinburgh, Western General Hospital, Edinburgh. EH4 2XU.
Tramoundanas AV, Clarkson AN, Harrison JC, Sawant P, Jones GT, Kerr DS, Sammut IA University of Otago Faculty of Medicine, Dunedin, New Zealand Cardiovascular pathology is seen in both animals and humans after domoic acid DOM ; intoxication. Whether this damage is direct ie., cardiotoxic ; or indirect ie., CNS autonomic seizures ; is not known. This study investigated the effect of seizure induction following intraperitoneal i.p. 2mg kg ; or intrahippocampal i.h. 50 300pmoles ; bolus administration of DOM on the development of cardiac pathologies. Sprague-Dawley rats male; 250 350g ; receiving either i.p. or i.h. DOM were assessed behaviourally and shown to.
In the area of biotechnology, we have been more specific and have adopted the following commitment: Exploration of any kind involves risk. And every risk must be anticipated and managed. "Our future is to turn discovery into value using the best scientific tools available. It is our responsibility to demonstrate that value, all the while assuring society that we can practice the technology safely." Charles O. Holliday, Jr., DuPont chairman & CEO New Technology At DuPont, we have always sought to minimize risk and maximize benefits. The same holds true for our work in biotechnology. Same Values We believe in the potential of biotechnology as one of several important tools to meet growing global needs. We have invested greatly in the belief that our traditional science, new biology tools and our strong market presence combine to give a competitive advantage. Fundamentally, our exploration is a business decision. But beyond the bottom line, and even more central to our day-to-day operations, are the values that drive our business decisions. Safety Begins at DuPont The solutions that built our business are based on enhancing, not harming, health and quality of life. Developed and refined over the past 200 years, scientific research and development at DuPont operate with careful processes to review risk, assess health and environmental impact, and stop development if and when safety is at issue. Our Record DuPont is on record as one of the most safety-conscious companies in the world. Other companies call on us to share our knowledge and safety performance practices. Our approach to biotechnology is no different. Scientific Approach As a global science company, DuPont uses a science-based framework to explore beneficial applications of biotechnology. We take seriously our responsibility and obligation to ensure that food and other products are rigorously tested and comply with governmental requirements and industry guidelines. In many cases DuPont even surpasses government requirements for health and environmental safety. A System for Safety DuPont employs a rigorous, science-based approach for a single goal -- your safety. In the case of food, the focus is on whether it is as safe and nutritious as the same item produced through conventional means. Highly trained DuPont scientists assess factors including characteristics of the plant variety, the possibility of unexpected or 15.
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When using fluorescence detection versus UV detection. The comparison of profiles is facilitated by the use of isoexcitation and emission plots. These colored "3D" diagrams give snapshots of time, wavelength, and either excitation or emission intensity. The profile comparisons are aided by the use of a complementary CE screen for inorganic anions and sugars. Tablets with similar physical characteristics can exhibit similar fluorescence and anion profiles potentially indicating common synthetic origin and tabletting material. Conversely, tablets with similar physical characteristics may also exhibit distinctly different anion and or fluorescence profiles, indicating different tabletting materials or different synthetic origin. Similarly, powders with comparable MDMA HCl content can exhibit different fluorescence profiles, indicating different synthetic origin. Due to the lower particle size columns 1.7 m ; , high pressure capability 15000 psi ; , and reduced dead volumes, UPLCTM affords higher peak capacity and lower separation times than conventional HPLC operating at 6000 psi. For MDMA profiling using photo diode array PDA ; UV detection, UPLCTM provides approximately twice the peak capacity of HPLC in approximately half the analysis time. UPLCTM, in combination with highly selective tandem MS detection, provides up to a 260X increase in signal-to-noise over PDA UV detection. This is accomplished using multiple reaction monitoring MRM ; , where specific parent daughter combinations are monitored in the static mode. MDMA, Profiling, Liquid Phase Separations.
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