Legends for figures Fig. 1. Time-profiles of the plasma concentration of topotecan in mice given different oral doses of Pluronic P85 or Tween 20. Mice were given an oral dose of Pluronic P85 100, 250 and 500 mg kg ; A ; or Tween 20 50, 100 and 250 mg kg ; B ; , 15 min before an oral dose of topotecan 1 mg kg ; . The plasma concentration of topotecan was determined at designated times. Each point and bar represents the mean S.D. n 3-6 ; . Where vertical bars are not shown, the S.D. was within the size limit of the symbol. * p 0.05; * p 0.01, significant difference between with and without excipients.
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Suthat Fucharoen, MD, an internationally recognized scientist who specializes in thalassemia, iron overload and genetic modifiers of disease paid a special visit to Children's. Dr. Fucharoen gave a talk on "Searching for Disease Modifier Genes in Beta Thalassemia HbW." We would like to extend our sincere thanks for his time and for sharing his expertise with us.
BARVE RM, GHONGANE BB, YEGNANARAYAN R Dept. of Pharmacology, B.J. Medical College, Pune-411001. Objective: To study the pattern of non-prescription dispensing by interviewing customers visiting chemist's shop to purchase medicines.
Response24 Response rate In total, 202 participants were evaluated for response, 96 in the topotecan group and 106 in the paclitaxel group. All participants who were not fully assessed for efficacy or who were not evaluated were considered to be non-responders.
Topotecan, respectively [18, 20]. Neutropenia was noncumulative, and the incidence of grade 4 neutropenia decreased after the use of G-CSF, indicating that grade 4 neutropenia associated with topotecan treatment is manageable. Grade 4 thrombocytopenia and anemia were experienced by 25% and 4%, respectively, of patients treated with topotecan. The median onset of grade 4 neutropenia in patients treated with topotecan in the ten Bokkel Huinink et al. [18] study occurred on day 9, with a median duration of 6 days. In a combined population of relapsed ovarian and small cell lung cancer patients, the median onset of grade 4 neutropenia was similar. The median neutrophil and platelet nadirs for this combined population by treatment cycle are shown in Figure 2 [19]. After the first cycle, patients may have received G-CSF support or reduced doses of topotecan, and some may have discontinued topotecan due to myelosuppression. In general, grade 4 neutropenia had an onset of 10 days with a nadir at 12 days and a duration of 7 days [19]. Grade 4 thrombocytopenia had an onset and nadir at 15 days and a duration of 5 days. Grade 3 4 anemia had an onset of 13 days with nadir at 15 days and duration of 6 days. The profile of this myelosuppression reflects the noncumulative nature of the grade 3 4 neutropenia and thrombocytopenia experienced by patients treated with topotecan, as the platelet and neutrophil nadirs were less severe in subsequent cycles once an appropriate dose level was found. Myelosuppression and many of the nonhematologic toxicities of topotecan, such as fatigue, rash, and diarrhea, may be affected by the patient's renal function. Renal excretion is important for the elimination of topotecan, with 28%-68% of a dose eliminated by the kidneys. O'Reilly et al. [22] studied the pharmacokinetics and pharmacodynamics of topotecan in patients with normal renal function and varying degrees of renal dysfunction. Results indicated that both the creatinine clearance and the extent of prior treatment were predictive of the severity of hematologic toxicity and need and toradol.
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Wong, Berkenblit CNS. These anecdotal observations provided a basis for topotecan chemoirradiation investigations for the treatment of brain metastases. The feasibility of topotecan in combination with cranial irradiation was rigorously investigated in one phase I and one phase II study of patients with glioblastoma multiforme [56, 57]. In the phase I study, systemic toxicities, primarily hematologic, were tolerable up to the standard topotecan dose of 1.5 mg m2 day in combination with cranial irradiation [56]. In the phase II study, patients received topotecan at doses of 1.5 mg m2 day on days 1-5 of a 21-day cycle and standard cranial radiation therapy 60 Gy in fractions over 6 weeks ; [57]. Although there was no statistically significant survival advantage of this therapy over other therapies, the combination of topotecan and radiotherapy was generally well tolerated. Only two 2% ; patients experienced grade 4 CNS neurotoxicity decreased responsiveness ; and four 5% ; patients had grade 3 CNS neurotoxicity headache, decreased motor function, confusion, agitation, hallucination, and visual disturbance ; within 90 days of radiation therapy. Only two 2% ; patients experienced delayed 90 days ; grade 3 CNS neurotoxicity. In another phase I II study, Grschow et al. [58] investigated the feasibility of topotecan in combination with radiotherapy in patients with brain metastases. Patients were treated with a continuous i.v. infusion of topotecan at a dose of 0.4-0.6 mg m2 day for 21 days in combination with whole-brain cranial irradiation in 2.0 Gy fraction ; . Of 13 evaluable patients, four had CRs, two had PRs, and six had SD within the CNS. Intracerebral recurrence was reported in two patients, 4 months and 9 months after and toremifene
FIGURE 2 The relationship between Ca2 + -Mg2 + ATPase and the total phospholipid n-6 n-3 polyunsaturated fatty acid ratio and membrane total lipid unsaturation index in cardiac sarcoplasmic reticulum. A ; Relative activity of Ca2t-Mg2 ATPase versus total phospholipid n-6 n-3 PUFA ratio. Data are presented as the relative activity of ATP hydrolysis with the corn oil group arbitrarily set at 100 and all other groups compared to this value for ATPase activity. The n-6 n-3 PUFA ratio represents the 2 n-6 fatty acids ; 2 n-3 fatty acids ; of SR total phospholipids. Each point represents the mean SEM, n 3 pools of 3 hearts per replicate ; . B ; Relative activity of Ca2 + -Mg2 + ATPase versus membrane total lipid unsaturation index. Data for the unsaturation index are pre sented as 2 mole percent of each fatty acid ; x number of double bonds associated with each fatty acid ; in the total lipid of mouse cardiac SR, and with relative activity with the corn oil group arbitrarily set at 100 and all other groups then com pared to this value. Each value represents the mean SEM, n 3 pools of 3 hearts per replicate.
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We hypothesized that OATs mediate the basolateral uptake of topotecan hydroxyl acid in renal epithelial cells. Therefore, in the present study, we and torsemide.
5. Catimel G, Vermorken JB, Clavel M et al. A phase II study of gemcitabine LY 188011 ; in patients with advanced squamous cell carcinoma of the head and neck. Ann Oncol 1994; 5: 543-7. Theodossiou C, Cook JA, Fisher J et al. Interaction of gemcitabine with paclitaxel and cisplatin in human tumor cell lines. Int J Oncol 1998; 12: 825-32. Jensen PB, Holm B, Sorensen M. In vitro cross resistance and collateral sensitivity in seven resistant small-cell lung cancer cell lines. Preclinical identification of suitable drug partners to Taxotere, topotecan and gemcitabine Br J Cancer 1997; 75: 869-77. Fountzilas G, Papadimitriou V, Bafaloukos D et al. Paclitaxel and carboplatin as first-line chemotherapy for advanced breast cancer. Oncology 1998; 12 Suppl 1 ; : 45-8.
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| Topotecan small cell lungVariant" to differentiate it from the petit mal absence seizures associated with rhythmic spike-and-waves 1 ; . In 1950, Lennox and Davis found clinical correlation between this type of EEG and patients with multiple epileptic crisis 2 ; . Based upon the contributions of Lennox and colleagues, Gastaut 3 ; and Dravet and colleagues of the Marseille school, the term "Lennox-Gastaut Syndrome" LGS ; was adopted. Diagnosis criteria definition LGS belongs to the group of severe infantile epileptic syndromes epileptic neonatal encephalopathy with suppression-burst, West syndrome, severe myoclonic epilepsy of infancy ; , which represent the most distressing epileptic encephalopathies of infancy. LGS is characterized by the following symptomatic triad: several epileptic seizures atypical absences, axial tonic seizures and sudden atonic or myoclonic falls diffuse slow interictal spike wave in the waking EEG 3 Hz ; and fast rhythmic bursts 10 Hz ; during sleep; slow mental development associated with personality disturbances. Although this last element is not indispensable for the diagnosis, it is manifested in a high percentage of cases 4 ; . LGS is a controversial entity due to the difficulty of establishing its semiological electroclinical features and some authors have considered that severe cases of myoclonic astatic epilepsy represent myoclonic variants of LGS 4; 5 ; . However the myoclonic phenomenon is not predominant in LGS, and this review focuses only on Lennox-Gastaut syndrome, as strictly defined above. LGS is defined by the International Classification of Epilepsies, Epileptic Syndromes, and Related Seizure Disorders as a cryptogenic or symptomatic generalized epilepsy 6 ; . Differential diagnosis All the epilepsies with frequent and brief seizures occurring in childhood should be eliminated from differential diagnosis: Myoclonic epilepsies - Benign atypical partial epilepsy of the childhood - Partial post-traumatic epilepsy with slow spikewave - ESES syndrome - Rett syndrome - Angelman syndrome Epilepsy absence with tonic or atonic component. Landau-Kleffner syndrome Multifocal severe epilepsy Ceroid-lipofuscinosis Gobbi syndrome epilepsy, celiac disease and occipital calcifications.
Topotecan ovarian cancer 4mg m2
ATS CDC IDSA. Treatment of TB. J Respir Crit Care Med 2003; 167: 603-662. CDC. Core Curriculum on Tuberculosis. U.S. Department of Health and Human Services-Public Health Service, Fourth edition, 2000 : cdc.gov nchstp tb pubs corecurr default ; . Garay SM, Rom, WN. Tuberculosis. Little, Brown and Company; 2nd edition 2003. Iseman MD. A Clinicians Guide to Tuberculosis. Lippincott Williams and Wilkins 2000 and tranylcypromine.
40 Cass I, Kuo DY, Fields AL et al. Profound thrombocytopenia in previously treated patients with recurrent ovarian carcinoma receiving topotecan. Gynecol Oncol 1998; 69: 175-178. Duffull SB, Robinson BA. Clinical pharmacokinetics and dose optimisation of carboplatin. Clin Pharmacokinet 1997; 33: 161-183. Budd GT, Ganapathi R, Wood L et al. Approaches to managing carboplatin-induced thrombocytopenia: focus on the role of amifostine. Semin Oncol 1999; 26 suppl 7 ; : 41-50. 43 Rowinsky EK, Kaufmann SH, Baker SD et al. Sequences of topotecan and cisplatin: phase I, pharmacologic, and in vitro studies to examine sequence dependence. J Clin Oncol 1996; 14: 30743084. Balducci L, Phillips DM, Davis KM et al. Systemic treatment of cancer in the elderly. Arch Gerontol Geriatr 1988; 7: 119-150. O'Reilly S, Rowinsky E, Slichenmyer W et al. Phase I and pharmacologic studies of topotecan in patients with impaired hepatic function. J Natl Cancer Inst 1996; 88: 817-824. Jelliffe RW. Letter: creatinine clearance: bedside estimate. Ann Intern Med 1973; 79: 604-605. Cockcroft DW, Gault MH. Prediction of creatinine clearance from serum creatinine. Nephron 1976; 16: 31-41. O'Reilly S, Armstrong DK, Grochow LB. Life-threatening myelosuppression in patients with occult renal impairment receiving topotecan [letter]. Gynecol Oncol 1997; 67: 329-330. Rodriguez M, Rose PG. Improved therapeutic index of lower dose topotecan chemotherapy in recurrent ovarian cancer. Gynecol Oncol 2001; 83: 257-262. Aravantinos G, Zafiropoulos A, Bafaloukos D et al. Topotecan in heavily pretreated platinum resistant ovarian cancer patients. Presented at the 10th Symposium of New Drugs in Cancer Therapy, Amsterdam, June 16-19, 1998: 67. Nielsen HA, Nielsen D, Engelholm SA. Effect of topotecan on serum CA-125 in patients with advanced epithelial ovarian cancer. Gynecol Oncol 2000; 77: 383-388. Gronlund B, Hansen HH, Hogdall C et al. Efficacy of lowdose topotecan in second-line treatment for patients with epithelial ovarian carcinoma. Cancer 2002; 95: 1656-1662. Gordon A, Bookman M, Malmstrom H et al. Efficacy of topotecan in advanced epithelial ovarian cancer after failure of platinum and paclitaxel: International Topotecan Study Group trial. Proc Soc Clin Oncol 1996; 15: 282. Goldwasser F, Buthaud X, Gross M et al. Decreased topotecan platelet toxicity with successive topotecan treatment cycles in advanced ovarian cancer patients. Anticancer Drugs 1999; 10: 263-265. Brown JV 3rd, Peters WA 3rd, Rettenmaier MA et al. A phase I trial of a 3-day topotecan Q 21 days for recurrent epithelial cancers of the ovary, fallopian tube, and peritoneum. Gynecol Oncol 2000; 79: 495-498. Clark RS, Fracasso PM, Picus J. A phase I study of weekly topotecan as a bolus infusion. Proc Soc Clin Oncol 1999; 18: 207a. Morris R, Munkarah A. Alternate dosing schedules for topotecan in the treatment of recurrent ovarian cancer. The Oncologist 2002; 7 suppl 5 ; : 29-35 and topotecan.
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Such a weapon was to deter the Germans in the event they succeeded in also doing so. When Rotblat realized in late 1944 that the Germans would not succeed in this attempt, he left the US atomic bomb project at Los Alamos, New Mexico, and returned to London. He was the only Manhattan Project scientist to leave the project on principle, and he would spend the rest of his life working to eliminate nuclear weapons and war. He would never again work on creating a weapon, and spent the remainder of his career working as a physicist at St. Bartholomew's Hospital in London. Joseph Rotblat was born in Warsaw, Poland, in 1908. At the age of 30, he accepted a fellowship and went to London to work with physicist and and treprostinil.
Table 4. Response rate Response after paclitaxel 43 patients ; Response after topotecan 32 patients ; CR CR, n 1 PR, n 20 SD, n 11 PD, n 9 NA, n 2 ORR to paclitaxel, n 21 49% ; 1 0 0.
Summary of effectiveness data The effectiveness evidence for PLDH and topotecan was derived from trial 30-49. Study characteristics and results have been described earlier see `Summary of effectiveness data' in the review of the study by Smith and colleagues, 50 p. 66 ; . Summary of resource utilisation and costs data Data for resource utilisation from trial 30-49 were combined with the audit of current practice for relapsed ovarian cancer in the UK. The submission justified this approach on the basis that the audit was considered more representative of UK management of patients with epithelial ovarian cancer than a clinical trial and triac.
E, Gemetzi C, Kouroumalis E, Martin PM, Castanas E. Wine antioxidant polyphenols inhibit the proliferation of human prostate cancer cell lines. Nutr Cancer 2000; 37: 223-233 Iwashita K, Kobori M, Yamaki K, Tsushida T. Flavonoids inhibit cell growth and induce apoptosis in B16 melanoma 4A5 cells. Biosci Biotechnol Biochem 2000; 64: 1813-1820 Uddin S, Choudhry MA. Quercetin, a bioflavonoid, inhibits the DNA synthesis of human leukemia cells. Biochem Mol Biol Int 1995; 36: 545-550 Caltagirone S, Rossi C, Poggi A, Ranelletti FO, Natali PG, Brunetti M, Aiello FB, Piantelli M. Flavonoids apigenin and quercetin inhibit melanoma growth and metastatic potential. Int J Cancer 2000; 87: 595-600 Sliutz G, Karlseder J, Tempfer C, Orel L, Holzer G, Simon MM. Drug resistance against gemcitabine and topotecan mediated by constitutive hsp70 overexpression in vitro: implication of quercetin as sensitiser in chemotherapy. Br J Cancer 1996; 74: 172-177 Yang CS, Landau JM, Huang MT, Newmark HL. Inhibition of carcinogenesis by dietary polyphenolic compounds. Annu Rev Nutr 2001; 21: 381-406 Wang HK. The therapeutic potential of flavonoids. Expert Opin Investig Drugs 2000; 9: 2103-2119 Asaum J, Matsuzaki H, Kawasak S, Kuroda M, Takeda Y, Kishi K, Hiraki Y. Effects of quercetin on the cell growth and the intracellular accumulation and retention of adriamycin. Anticancer Res 2000; 20: 2477-2483 Damianaki A, Bakogeorgou E, Kampa M, Notas G, Hatzoglou A, Panagiotou S, Gemetzi C, Kouroumalis E, Martin PM, Castanas E. Potent inhibitory action of red wine polyphenols on human breast cancer cells. J Cell Biochem 2000; 78: 429-441 Yamashita N, Kawanishi S. Distinct mechanisms of DNA damage in apoptosis induced by quercetin and luteolin. Free Radic Res 2000; 33: 623-633 Musonda CA, Helsby N, Chipman JK. Effects of quercetin on drug metabolizing enzymes and oxidation of 2', 7-dichlorofluorescin in HepG2 cells. Hum Exp Toxicol 1997; 16: 700-708 Exon JH, Magnuson BA, South EH, Hendrix K. Dietary quercetin, immune functions and colonic carcinogenesis in rats. Immunopharmacol Immunotoxicol 1998; 20: 173-190 Drewa G, Wozqak A, Palgan K, Schachtschabel DO, Grzanka A, Sujkowska R. Influence of quercetin on B16 melanotic melanoma growth in C57BL 6 mice and on activity of some acid hydrolases in melanoma tissue. Neoplasma 2001; 48: 12-18 Weber G, Shen F, Yang H, Prajda N, Li W. Regulation of signal transduction activity in normal and cancer cells. Anticancer Res 1999; 19: 3703-3709 Weber G, Shen F, Prajda N, Yeh YA, Yang H, Herenyiova M, Look KY. Increased signal transduction activity and down-regulation in human cancer cells. Anticancer Res 1996; 16: 3271-3282 Richter M, Ebermann R, Marian B. Quercetin-induced apoptosis in colorectal tumor cells: possible role of EGF receptor signaling. Nutr Cancer 1999; 34: 88-99 Shen F, Herenyiova M, Weber G. Synergistic down-regulation of signal transduction and cytotoxicity by tiazofurin and quercetin in human ovarian carcinoma cells. Life Sci 1999; 64: 1869-1876 Levine AJ. p53, the cellular gatekeeper for growth and division. Cell 1997; 88: 323-331 Greenblatt MS, Bennett WP, Hollstein M, Harris CC. Mutation in the P53 tumor supressor gene: clues to cancer etiology and molecular pathogenesis. Cancer Res 1994; 54: 4855-4878 Hui AM, Makuuchi M, Li X. Cell cycle regulators and human hepatocarcinogenesis. Hepatogastroenterology 1998; 45: 1635-1642 Yang CS, Landau JM, Huang MT, Newmark HL. Inhibition of carcinogenesis by dietary polyphenolic compounds. Annu Rev Nutr 2001; 21: 381-406 Hollman PC, Katan MB. Health effects and bioavailability of dietary flavonols. Free Radic Res 1999; 31 Suppl ; : S75-80 Avila MA, Velasco JA, Cansado J, Notario V. Quercetin mediate the down-regulation of mutation p53 in the human breast cancer call line MDA-MB468. Cancer Research 1994; 54: 2424-2428 Thottassery, Zambetti GP, Arimori K, Schuetz EG, Schuetz JD and toradol.
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Note: the figure shows the percentage of patients whose hepatitis c treatment extended for 12 months or less, or for various durations beyond 12 months and triazolam
6. Conclusions and Recommendations In the present study, higher prevalence of cryptosporidiosis, giardiasis and amebiasis has been found among children below 14 years old with an average prevalence rate of 11.9%, 38% and 33.7%, respectively. An increasing prevalence in this study was associated with factors such as scarcity of water for consumption, indiscriminate defecation by the inhabitants and their animals, geographical settings of an area which is mountainous so whenever the rain comes it washes out waste products of human and other animals to their farm and surrounding ; , absence of toilet, keeping of livestock waste products in their backyards, living in overcrowded situations with many children per household coupled with poor sanitation, poor personal hygiene and high illiteracy. In addition a common practice of keeping certain domestic animals within or in close vicinity of house holds and many other factors contribute to the high prevalence of those parasites among children in Rural Dire-Dawa, Ethiopia. This study also indicated that cryptosporidiosis, giardiasis and amebiasis were seasonal diseases in the sense that their prevalence was higher during wet seasons and lower during dry seasons. Although significant difference was not obtained in the prevalence among children using protected and unprotected water sources in Legedini and Legebira, this does not mean that water development project does not have a role in reducing illness as a result of waterborne parasites; rather this water development should be conducted side by side with other discipline particularly with health sector. In addition untreated protected drinking water sources are not free of the waterborne parasitic pathogens. It was estimated that the prevalence of C. parvum does not vary between infants below 1 year old and in children with age group between 1 and 5 and between 6 and 14, but G. lamblia and Entamoeba histolytica was seen to increase with age. However, for Giardia, the rate increased till some point and reduces as children become older. On the contrary sex related prevalence of giardiasis, cryptosporidiosis and amebiasis were not observed in this study, which implies male.
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