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1. Rosenberg S. The management of Hodgkin's disease: half a century of change. The Kaplan memorial lecture. Ann Oncol 1996; 7: 555560. Ng AK, Bernardo MP, Weller E et al. Long-term survival and competing causes of death in patients with early-stage Hodgkin's disease treated at age 50 or younger. J Clin Oncol 2002; 20: 21012108. Aleman BM, van den Belt-Dusebout AW, Klokman WJ et al. Longterm cause-specific mortality of patients treated for Hodgkin's disease. J Clin Oncol 2003; 21: 34313439. Henry-Amar M. Second cancer after the treatment for Hodgkin's disease: a report from the International Database on Hodgkin's Disease. Ann Oncol 1992; 3 Suppl 4 ; : 117128. 5. Tucker M, Coleman C, Cox R. Risk of second cancers after treatment for Hodgkin's disease. N Engl J Med 1988; 318: 76 van Leeuwen FE, Chorus AM, van den Belt-Dusebout AW et al. Leukemia risk following Hodgkin's disease: relation to cumulative dose of alkylating agents, treatment with teniposide combinations, number of episodes of chemotherapy, and bone marrow damage. J Clin Oncol 1994; 12: 10631073. Josting A, Wiedenmann S, Franklin J et al. Secondary myeloid leukemia and myelodysplastic syndromes in patients treated for Hodgkin's disease: a report from the German Hodgkin's Lymphoma Study Group. J Clin Oncol 2003; 21: 34403446. Rueffer U, Josting A, Franklin J et al. Non-Hodgkin's lymphoma after primary Hodgkin's disease in the German Hodgkin's Lymphoma Study Group: incidence, treatment, and prognosis. J Clin Oncol 2001; 19: 20262032. Enrici R, Anselmo A, Iacari V et al. The risk of non-Hodgkin's lymphoma after Hodgkin's disease, with special reference to splenic treatment. Haematologica. 1998; 83: 636644.
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19. Torchia, E. C., R. J. Shapiro, and L. B. Agellon. Reconstitution of bile acid transport in the rat hepatoma McArdle RH-7777 cell line. Hepatology 24: 206211, 1996. Van Dyke, R. W., J. E. Stephens, and B. F. Scharschmidt. Bile acid transport in cultured rat hepatocytes. Am. J. Physiol. 243 Gastrointest. Liver Physiol. 6 ; : G484G492, 1982. 21. Von Dippe, P., M. Amoui, R. H. Stellwagen, and D. Levy. The functional expression of sodium-dependent bile acid transport in Madin-Darby canine kidney cells transfected with the cDNA for microsomal epoxide hydrolase. J. Biol. Chem. 271: 1817618180, 1996. Zimmerli, B., J. Valantinas, and P. J. Meier. Multispecificity of Na -dependent taurocholate uptake in basolateral sinusoidal ; rat liver plasma membrane vesicles. J. Pharmacol. Exp. Ther. 250: 301308, 1989. Bottom Line Health interviewed Jonny Bowden, a board-certified nutrition specialist based in Los Angeles and the author of Living the Low Carb Life Sterling ; . jonnybowden.
An antiviral drug, cidofovir Vistide ; , developed for the treatment of cytomegalovirus in AIDS, has broad activity to other viruses, including those in the pox family. Moreover, an often-seen skin complication of HIV disease caused by pox viruses is molluscum contagiosum. We have treated severe and resistant molluscum lesions successfully with the topical form of cidofovir. Cidofovir is administered intravenously. Its use is complicated by the fact that physicians should be thoroughly knowledgeable regarding its protocol for administration. The coadministration of probenicid and intravenous fluids are a necessary part of treatment because of possible harmful side effects to the kidneys. Because cidovovir is long-acting, the potential treatment for smallpox infection or exposure may only necessitate one dose. However, no testing in humans has been published. There is ongoing research proposed for the possible role of cidofovir in combating bioterrorism. Currently we are not prepared to deal with the potential emergency of a smallpox epidemic. Housing in motels has been proposed for patients exposed to smallpox. The modes of death due to smallpox occurs with bleeding lesions and internal bleeding that may progress to shock and death. Motels would not be the best place to deal with this. A single case is a global emergency. Much planning is in the works. A great deal is being learned while maneuvering through a maze of issues never before encountered. Most of the learning and decision-making occurs in an incremental way, piece by piece. Clearly, new protocols and expertise need to be in place in more areas than could be imagined. Early response is crucial. Expertise needs to encompass many scientific fields. A full-scale response should include public education that does not ignore immune compromised individuals. Appropriate prevention for them needs to be considered, since their exposure can lead to rapid disease progression. e Daniel S. Berger, MD is Medical Director for NorthStar Healthcare, Clinical Assistant Professor of Medicine at the University of Illinois at Chicago and editor of AIDSInfosource aidsinfosource ; . He also serves as medical consultant and columnist for Positively Aware. Dr. Berger can be reached at DSBergerMD aol or 773 ; 296-2400. Received 7 19 02; revised 9 16 02; accepted 9 19 02. Supported by grants from the National Cancer Institute Grants R01CA54422, RO1-CA89352, and P01-CA13330 ; , Aventis Pharmaceuticals, and UJA-Federation of New York. 2 To whom requests for reprints should be addressed, at Department of Oncology, Albert Einstein Cancer Center, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467. E-mail: eschwart aecom.yu and tenofovir. Animals and diets This study employed a typical depletion-repletion design for understanding the potential interactions of iron and zinc during supplementation in iron- and zincdeficient rats. The Institutional Animal Ethical and Biosafety Committee of the National Institute of Nutrition approved the study. Twenty-four weanling female Wistar-Kyoto rats, National Center for Laboratory Animal Science at the National Institute of Nutrition, Hyderabad, India ; weighing 35-45 g, were fed an egg-albumin-based, semisynthetic, purified iron- and zinc-deficient diet 6.5 mg Fe and 4.0 mg Zn kg diet ; for 4 wk Table 1 ; . Rats were housed individually in polypropylene cages with stainless steel wire floors 45 cm 16 cm, 7.5 mm mesh, 1 mm wire diameter ; to prevent coprophagy, in a room maintained at 23 and 60% humidity, with a 12-h light: dark cycle ; . Deionized distilled water, in plastic bottles with stainless steel sippers, was freely available to all rats. Body weight was recorded weekly and blood was collected by orbital sinus puncture for determination of iron and zinc status at the end of depletion and repletion. Oral repletion of iron and or zinc At the end of depletion phase, rats were randomly divided into three groups and assigned to either Fe, Zn and Fe + Zn groups for repletion n 8, each ; . In order to achieve complete repletion of both the minerals, while minimizing the intestinal oxidative damage, we used a dose of 4 mg iron and 3.3 mg zinc for repletion. Force feeding was performed daily during the repletion period, either with a dose of 4.0 mg iron Fe group ; , 3.3 mg zinc Zn group ; or a combination of 4.0 mg iron and 3.3 mg zinc Fe + Zn group ; in 1.0 mL 0.01 mol L HCl, via an orogastric plastic tube, for 2 wk [12]. During this period, the rats were fed an iron- and zinc-deficient diet ad libitum. The doses were prepared by dissolving FeSO4 and ZnSO4 salts, either individually or in combination, in dilute HCl[8]. Administration of 0.01 mol L HCl alone to the rats had no significant effect on the parameters.
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Lysates followed by CsCl ethidium isopycnic centrifugation and gel filtration on an A-50m column. VM-26 teniposide ; was a gift from Bristol-Myers Co. Media and fetal bovine serum for cell culture work were purchased from GIBCO. Rabbit antisera against purified calf Mammalian DNA topoisomerase I1 is the primary cellular thymus DNA topoisomerase I and I1 were prepared as described target of a number of potent antitumor drugs with diverse previously 11, 12 ; . Cells and Virus-Mouse erythroleukemia cells MELC ; were grown and unrelated chemical structures for a review, see Ref. 1 ; . Examples of these drugs, referred toas topoisomerase I1 in RPMI medium 1640. Monkey kidney cells BSC-1 ; were grown in Eagle's minimum essential medium. poisons, include acridines e.g. 4`- 9-acridinylamino ; -meth- with 10%heat-inactivated fetalbovineAll media were supplemented serum, 100 units ml penicillin, anesulfon-rn-anisidide ; , anthracyclines e.g. adriamycin and 100 pg ml streptomycin, and 2 m glutamine. The infection of BSCM daunomycin ; , anthracenediones e.g. mitoxantrone and bis- 1 cells with SV40 virus was carried out as described previously 9 ; . antrene ; , ellipticines e.g. ellipticine and 2-methyl-9-hy- Confluent BSC-1 cells were infected with an SV40 viral stock strain droxyl-ellipticinium acetate ; , and actinomycins e.g. actino- 776 ; at a multiplicity of infection of 10-30 plaque-forming units cell. mycin D ; , all of which are DNA intercalators and epipodo- Virus-infected cells were maintained in Eagle's minimum essential phyllotoxins e.g. demethylepipodophyllotoxin ethylidene-p- medium with 2% fetal bovine serum. Topoisomerase II Cleavage Assays-Topoisomerase I1 cleavage asD-glucoside and VM-26 ; ' which do not show significant DNA says were done as described previously 7-10 ; . Briefly, pBR322 DNA binding and are not DNA intercalators 1 ; .In mammalian was linearized with EcoRI and then end-labeled at the 3' termini cells, these drugs produce a common cellular DNA lesion with the large fragment of Escherichia coli DNA polymerase I in the other which is detected as protein-linked DNA breaks upon cell presence of [cY-~'P]~ATP and three unlabeled deoxyribonuclelysis with SDS or alkali 2-4 ; . The cellular protein which is otide triphosphates. Topoisomerase I1 cleavage reactions were done covalently linked to broken DNA strands has been identified in reaction mixtures 20 r l each ; containing Tris 40 mM, pH 7.5 ; , KC1 100 mM ; , MgClz 10 mM ; , dithiothreitol 0.1 mM ; , EDTA 0.5 to be topoisomerase I1 5, 6 ; . How topoisomerase I1 mediates mM ; , bovine serum albumin 30 pglml ; , HeLa DNA topoisomerase the drug action has recently been suggested from studies using I1 20 ng ; , and end-labeled [3ZP]pBR322 DNA 10 ng ; . Reactions were purified mammalian DNA topoisomerase I1 7-9 ; . All these incubated at 37 `C for 30 min. For heat reversal, the incubated drugs interfere with the breakage-reunion reaction of topoi- reaction mixture was then heated to 65 "C for specified times. Reacsomerase I1 by trapping a tight possibly covalent ; enzyme- tion were terminated by 10% SDS 1p1 ; and proteinase K 1.7 mg DNA complex, termed the "cleavable complex, " which is ml, 1 pl ; , and further incubated at 37 "C for 1 h. DNA samples were on a 1%agarose presumed to be the key covalent intermediate or one related analyzed2.0 mM EDTA ; . gel in TBE buffer 89 mM Tris borate pH 8.3 ; and to it in the topoisomerase strand-passing reaction pathway Immunoblot Analysis of Topoisomerase Contents-Immunoblot 10 ; . The formation of this putative enzyme-DNA-drug ter- analysis using rabbit antisera against human topoisomerase I and I1 nary complex is reversible and apparently aborts the strand- was done with minor modifications as described previously 12, 13 ; . Potassium-SDS Co-precipitation Assay-Potassium-SDS co-pre * This work wassupported by National Institutes of Health Grants cipitation assays, both in the purified system and in drug-treated GM-27731 and CA-39962. The costs of publication of this article cells, were done as described previously 6, 10 ; . were defrayed in part by the payment of page charges. This article RESULTS AND DISCUSSION must therefore be hereby marked "aduertisement" in accordance with 18 U.S.C. Section 1734 solelyto indicate this fact. Exposure of topoisomerase I-DNA cleavable complexes to The abbreviations used are: VM-26, 4'-demethylepipodophyllotoxin thenylidene-P-D-glucoside; SDS, sodium dodecyl sulfate; an elevated temperature e.g.65 " C ; has been shown to abolish MELC, murine erythroleukemia cells. subsequent DNA cleavage upon addition of a strong protein. References 1. Hofmann MA, Kohl B, Zumbach MS, Borcea V, Bierhaus A, Henkels M, Amiral J, Fiehn W, Ziegler R, Wahl P, Nawroth PP: Hyperhomocyst e ; inemia and endothelial dysfunction in IDDM. Diabetes Care 20: 18801886, 1997 The version of this paper cited here was withdrawn. A revised version was printed in Diabetes Care 21: 841848, 1998. ; 2. Colwell JA: Elevated plasma homocysteine and diabetic vascular disease. Diabetes Care 20: 18051806, 1997 Robillon JF Canivet B, Candito M, Sadoul , JL, Jullien D, Morand P, Chambon P, Freychet P: Type 1 diabetes mellitus and homocyst e ; ine. Diabete Metab 20: 494496, 1994 Munshi M, Stone A, Fink L, Fonseca V: Hyperhomocysteinemia following a methionine load in non-insulin dependent diabetes and macrovascular disease. Metabolism45: 133135, 1996 5. Fonseca VA, Mudaliar S, Schmidt B, Fink LM, Kern PA, Henry RR: Plasma homocysteine concentrations are regulated by acute hyperinsulinemia in diabetic but not type II diabetic subjects. MetabolismIn press . 6. Bostom AG, Brosnan JT, Hall B, Nadeau MR, Selhub J: Net uptake of plasma homocysteine by the rat kidney in vivo. Atherosclerosi116: 5962, 1995 s 7. Fonseca VA, Stone A, Munshi M, Baliga BS, Aljada A, Thusu K, Fink L, Dandona P: Oxidative stress in diabetes mellitus: does homocysteine have a role? South Med J 90: 903906, 1997 Guba S, Fonseca V, Fink L: Hyperhomocysteinemia: the emerging and important risk factor for cardiovascular disease. J Clin Pathol106: 709722, 1996 and terfenadine.

Rather than exhaustively measure the exact "equivalent-luminance-contrast" of fixation-related inhibition caused by S-cone stimuli in different situations, the aim of Experiment 3 was to take advantage of the likely non-linearity in the luminance pathways e.g. Kaplan and Shapley 1986 ; to show that the relative "strength" of an S-cone stimulus and a given luminance stimulus can reverse from one simple condition to another. This would prove that the S-cone stimuli do not have a consistent "equivalent-luminance-contrast", and must therefore be transmitted by a different pathway. Experiment 3A measured the relative inhibitory effects of the S-cone and low luminance stimuli compared to a high luminance stimulus. In two of the conditions in Experiment 3A we employed fixation changes from low to high luminance, or vice versa. It was expected that the high luminance stimulus would cause the most fixation related inhibition, and thus saccade latencies would be greater following a low-to-high-luminance change at fixation compared to the high-to-low condition. The difference in mean latency between these conditions would be the measure of the relative difference in fixation-related inhibition caused by the two stimuli. We also employed fixation changes from the Scone stimulus to the high luminance stimulus, or vice versa. It was again expected that the high luminance stimulus would cause the most fixation related inhibition, and thus following the S-to-highluminance change at fixation, saccadic latencies would be longer than in the high-to-S condition. The key question was whether the difference in fixation-related inhibition between the high luminance and S-cone stimuli was greater or smaller than the inhibition difference between the high and low luminance stimuli. If it was smaller, then the S-cone stimulus would seem to create more fixation related inhibition than the low luminance stimulus Figure 3Ai ; . If it was larger, the S-cone stimulus would seem to create less inhibition than the low luminance stimulus Figure 3Aii ; . The relative amount of fixation-related inhibition elicited by the S-cone stimuli will be compared across Experiments 3A and 3B. If the S-cone stimuli cause fixation-related inhibition in the same manner as luminance stimuli, then the relative fixation-related inhibition elicited by the S-cone stimuli should not differ between Experiments 3A and 3B as indicated in Figure 3 ; . Therefore, in Experiment 3A we rank the Low luminance and S-cone stimuli in terms of their inhibitory effect, and in Experiment 3B we test whether this rank remains consistent in other conditions. Materials and Methods Participants. 8 participants were employed 3 male, 5 female, aged 22-24 ; . All subjects had normal or corrected to normal acuity and normal colour vision, and none had served in Experiments 1 or 2. Procedure All aspects of the apparatus, calibration, procedure, and analysis were identical to Experiments 1 and 2, except where specified below. In all trials there was a change in the fixation stimulus 200 ms before. Table 7. 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Of the 188 patients enrolled on Total XII, 182 achieved a complete remission. Their demographic characteristics have been described previously.5 The number of patients with pharmacologic variables measured and the total number of measurements are indicated in Table 1. TPMT was measured in 154 patients; 26 other patients never had an interpretable RBC TPMT measurement, but did have TGN measurements that were used to classify them as either TPMT homozygous wild-type or heterozygous individuals. Of the 182 patients achieving complete remission, two were homozygous mutants, 17 were heterozygotes, 161 were homozygous wild-type, and two were not classified because they had neither informative TPMT nor RBC TGN measured. TPMT genotype was evaluated in 28 patients and was in complete concordance with assigned phenotype 18 homozygous wildtype [all TPMT * 1 * 1], eight heterozygous [all TPMT * 1 * 3A], and two homozygous mutant individuals [one * 2 * 2, one * 3A * 2] ; . Descriptive summaries for TGNs, TIMP, MeTIMP, MTXPGs, methotrexate AUC, teniposide AUC, cytarabine AUC, 6MP dose intensity, methotrexate dose intensity, and RBC TPMT activity are provided in Table 1. Univariate analyses showed that the only factors associated with EFS for the entire follow-up period Table 1 ; were 6MP P .006 ; and methotrexate dose intensity P .039 ; . When the analysis was restricted to a follow-up period only extending to the end of the pulse therapy, higher methotrexate AUC was significantly P .0187 ; associated with improved EFS among the B-lineage cases, as previously reported.5 Because doses of 6MP were. Table C.1: Compositions of SS-316 Zircaloy-2 mixture vs. theoretical feed for fluorination scheme. 73 Table C.2: Pressure and major gaseous products from reaction of varying amounts of F2 gas with 50.3% SS-316 and 49.7% Zircaloy-2, at 100 C. 76 Table C.3: Major gaseous products from reaction of 50.3% SS-316 & 49.7% Zircaloy-2 with 14.6g F2 100C ; . 79 Table C.4: Gaseous products from reaction of F2 gas with SS-316 Zircaloy2, with varying amounts of initial air F2 . 84 Table C.5: Gaseous products from reaction of F2 gas with SS-316 Zircaloy2, with varying amounts of initial air Constant F2 ; . 85 and thiabendazole.
Age 65, give a single revaccination at age 65 or older ; if at least 5 years have elapsed since the previous dose. Nephrology, Department of Medicine, Technische Universitat Dresden, F.R.G and thiamin. Table 3. Prognostic Factors to Reach CR After ABMT. And FT, levels, although declining, were still at the upper limit of the normal range. Individual serum wSU levels and the calculated Y-SU TSH mr are presented in Table 2. Compared to 264 normal controls matched for circulating TSH and gonadotropin concentrations 17 ; , 11patients 64.5% ; had high Y-SU levels, and 13 76.5% ; had elevated Y-SU TSH mr Table 2 ; . It noteworthy that all 3 patients with microadenoma had normal CPSUlevels and r-SU TSH mr. Serum SHBG levels, available for 15 patients, were elevated in all patients with high FT, and FT4levels and in 1 of and thioguanine and teniposide. Daunorubicin daunoxome ; teniposide vumon.

Hemodynamic and ventilatory parameters were determined at baseline and maintained within normal limits throughout the experimental 4-h period. Left ventricular LV ; pressure was monitored with a 2F Millar Mikro-Tip catheter model SPC-320; Millar Instruments, Houston, TX ; placed via the left carotid artery before baseline measurements. The analog signal derived from the catheter was amplified, digitized, and processed with a CA Recorder Series II system DISS, Pinckney, MI ; . Cardiac contractility was assessed using the first derivative of LV pressure generation dP dT, mm Hg s ; at its maximal point and at a submaximal point 25 mm Hg generated pressure ; . LV relaxation time time in milliseconds required for the maximum negative dP dT to recover 50% back toward 0 mm Hg was also evaluated. Each measurement was determined from the mean value recorded over a 10-min steady state period and expressed as a percentage of a similar determination at baseline because of animal-to-animal variability and thiotepa.
Compounds with similar mechanisms of action and mutagenicity profiles have been reported to be carcinogenic and teniposide should be considered a potential carcinogen in humans. Gonzalo Abello Paz, Transient MMA, Age 3 .2 D2HGA & L2HGA Genetic Defects Discovered .3 Meredith Elyse Tyson, L-2 Hydroxyglutaric Acidemia, Age 15 years .4 Low Protein Resources .6 News From Cambrooke Foods .7 Martha Fick ; Duffy, Propionic Acidemia, Age 27 .8 Delany Sebo, Age 4-1 2, MMA Cbl B and Nathan Sebo, Age 6 months, MMA Cbl B .10 A Novel Form of Isovaleric Acidemia .12 N-Acetylglutamate Synthase Deficiency Can Potentially Be Cured with N-Carbamylglutamate .13 MMA and Related Disorders Program at NIH .13 Jordan McCann, Age 9, MMA mut 0 ; and Jenna McCann, Age 4, MMA mut 0 ; .14 Teegan Sakaguchi, Propionic Acidemia, Age 3 .15.

In vivo studies For certain drugs and dosage forms, in vivo documentation of equivalence, through either a bioequivalence study, a comparative clinical pharmacodynamic study, or a comparative clinical trial, is regarded as especially important. Examples are listed below. a ; Oral immediate release pharmaceutical products with systemic action when one or more of the following criteria apply: i ; ii ; indicated for serious conditions requiring assured therapeutic response; narrow therapeutic window safety margin; steep dose-response curve. Teniposide injection is used along with other medicines to treat acute lymphoblastic leukemia all ; , non-hodgkin's lymphoma nhl ; , and neuroblastom precautions source: medlineplus ; before taking teniposide, tell your doctor and pharmacist if you are allergic to teniposide or any other drugs. Teniposide ten-IP-aw-side ; is a drug that is used to treat many kinds of cancer. It is a clear liquid that is injected slowly into a vein. A blood sample will be taken before each treatment. The dose and timing of your chemotherapy may be changed based on your blood counts and or other side effects. Other drugs such as phenobarbital, phenytoin DILANTIN ; may interact with teniposide. Tell your doctor if you are taking these or any other drugs as your dose may need to be changed. Check with your doctor or pharmacist before you start taking any new drugs. The drinking of alcohol in small amounts ; will not affect the safety or usefulness of teniposide. Teniposide may damage sperm and may harm the baby if used during pregnancy. It is best to use birth control while being treated with teniposide. Tell your doctor right away if you or your partner becomes pregnant. Do not breast feed during treatment. Tell doctors or dentists that you are being treated with teniposide before you receive any treatment from them. SIDE EFFECTS Teniposide burns if it leaks under the skin. MANAGEMENT Tell your nurse or doctor immediately if you feel burning, stinging or any other change while the drug is being given. Tell your nurse or doctor immediately. Raise your feet if you are not already lying down. You may be given an antinausea drug with your treatment and a prescription to take at home. It is easier to prevent nausea than treat it once it has occurred, Follow antinausea drug directions closely. Drink plenty of liquids. Eat often in small amounts. Try the ideas in the For the Patient: Nausea. To help prevent infection: Wash your hands often and always after using the bathroom. Take care of your skin and mouth. Avoid crowds and people who are sick. Call your doctor immediately at the first sign and tenofovir. Differential effects of antihypertensive drug therapy on vascular smooth muscle cell hypertrophy, hyperploidy, and hyperplasia in the spontaneously hypertensive rat GK Owens Circ. Res. 1985; 56; 525-536.
No. of Patients With Cancer Stage III 72 17 IV Performance Status * 0-1 80 NA 2 21 Treatment Regimens Single Agent Vindesine Vindesine Doublet Vindesine plus cisplatin Vindesine plus cisplatin Detail Decreased dose of vindesine in investigational arm Trial with 2 comparisons, 3 arms; did not use intent-to-treat analysis; Karnofsky scores 50 Palliative radiotherapy or surgery possible Trial did not use intent-to-treat analysis; 120 mg m2 or 360 mg m2 of teniposide Trial with 3 arms, 2 eligible.