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Of treatments and disease progression, best response, and methods used for tumor measurement. Treatment Patients were randomly assigned to LV5FU2 or FOLFOX4. In the LV5FU2 arm, LV 200 mg m2 was administered via intravenous infusion for 2 hours, followed by FU 400 mg m2 bolus for 2 to 4 minutes, followed by FU 600 mg m2 via intravenous infusion for 22 hours on day 1. LV and FU were repeated on day 2. The same doses and schedule of FU LV were used in the FOLFOX4 arm, with the addition of oxaliplatin 85 mg m2 given for 2 hours at the same time as LV infusion ; before bolus FU on day 1. Regimens were repeated every 2 weeks until disease progression was radiologically documented, unacceptable toxicity occurred, patient refused to continue treatment, or the physician no longer considered treatment beneficial for the patient. Patients receiving LV5FU2 who experienced disease progression were allowed to cross over to treatment with FOLFOX4. All patients received antiemetics at the physician's discretion. Pretreatment with 5HT3 antagonists plus dexamethasone was recommended for patients receiving oxaliplatin. Use of colony-stimulating factors was not recommended for prophylaxis, but could be used in patients with poor prognostic factors. Response and Toxicity Assessments Tumor measurements by CT or MRI were repeated every 6 weeks during the study. Response Evaluation Criteria in Solid Tumors Group RECIST ; criteria were used to determine tumor response. Patients with complete CR ; or partial PR ; tumor response had confirmatory CT or MRI scans performed 4 to 6 weeks after achieving an initial objective response. CR was defined as the disappearance of all target and nontarget tumor lesions. PR was a 30% or greater decrease in the sum of the longest diameter of all target lesions, referenced against the baseline sum of the longest diameter of target lesions together with stabilization or decrease in size of nontarget lesions. Disease progression required a 20% increase in the sum of the longest diameter of target lesions, an unequivocal increase in the nontarget lesions, or appearance of any new lesions. Stable disease was defined as insufficient tumor shrinkage to qualify for PR and insufficient increase in tumor size to qualify for progressive disease.
Interstitial cystitis Bisphosphonate - prevention of skeletal events pathological fractures, bone complications requiring radiotherapy surgery ; in patients with breast cancer bone metastases - treatment of tumourinduced hypercalcaemia with without metastases. Imatinib Mesilate Management of chronic myeloid leukemia Imiglucerase Enzyme replacement - Gaucher's disease Indinavir Protease inhibitor; HIV infection Indocyanine dye Imaging in Ophthalmology Infliximab Rheumatoid arthritis, Crohn's disease Interferon alfa All licensed indications AIDS-related Kaposi's sarcoma, hairy cell leukaemia, lymph liver metastases of carcinoid tumour, chronic active hepatitis B, chron hep C, adjunct in malignant melanoma & maintenance of remission of multiple myeloma ; Interferon beta Multiple sclerosis Irinotecan Metastatic colorectal cancer used with 5-FU and folinic acid Isotretinoin Oral retinoid - acne Lamivudine Hepatitis B treatment, NRTI- HIV infection Lenograstim Recombinant human granulocyte-colony stimulating factor - neutropenia Linezolid Antibiotic Magnesium aspartate Hypomagnesaemia sachets Memantine Moderately severe to severe Alzheimers disease. Methotrexate IM ; All indications 5-Methoxypsoralen PUVA treatment of psoriasis Methylphenidate MR Another MR formulation which has different Equasym XL ; release characteristics to the product already in the shared care guidelines Molgramostim Recombinant human macrophage-colony stimulating factor - neutropenia Nabilone Antiemetic; Multiple sclerosis treatment Nafarelin Gonadorelin analogue - IVF Nelfinavir Protease inhibitor; HIV infection Nevirapine NNRTI - HIV infection Octreotide unlicen- Somatostatin analogue - unlicensed indications sed indications ; only Ostenil Mini Hyaluronic acid for Synovial Fluid Replacement Oxaliplatin Metastatic colorectal cancer used with 5-FU and folinic acid Palivizumab Antiviral to prevent lower respiratory tract infections by RSV in specific young children.
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Retinoids all-trans retinoic acid all-trans retinoic acid atra ; is a drug used for the treatment of acute promyelocytic leukemia aml subtype m3 ; vinca alkaloids and derivatives vinblastine vincristine vindesine vinorelbine vinblastine is a drug used to treat certain kinds of cancer, including lymphoma and breast cancer or testicular cance vincristine oncovin® is an alkaloid from the madagascar periwinkle catharanthus roseus, formerly vinca rosea and hence its name ; vinorelbine navelbine ; is a chemotherapy drug that is given as a treatment for some types of cancer including breast cancer and non-small-cell lung cance full alphabetical listing all-trans retinoic acid azacitidine azathioprine bleomycin carboplatin capecitabine cisplatin chlorambucil cyclophosphamide cytarabine daunorubicin docetaxel doxifluridine doxorubicin epirubicin etoposide fluorouracil gemcitabine hydroxyurea requires categorization idarubicin mechlorethamine mercaptopurine methotrexate mitoxantrone oxaliplatin paclitaxel teniposide thioguanine valrubicin vinblastine vincristine vindesine vinorelbine categories : incomplete lists chemotherapeutic agents all-trans retinoic acid atra ; is a drug used for the treatment of acute promyelocytic leukemia aml subtype m3 ; azathioprine is a chemotherapy drug, now rarely used for chemotherapy but more for immunosuppression in organ transplantation and autoimmune disease such as rheumatoid arthritis or crohns diseas bleomycin is an anti-cancer agen ; carboplatin is a chemotherapy drug used against some form of cance capecitabine - wikipedia * import w skins.
27 Wagener DJ. Verdonk HE, Dirix LY et al. Phase II trial of CPT11 in patients with advanced pancreatic cancer, an EORTC early clinical trials group study. Ann Oncol 1995; 6: 129-132. Fukuda M, Nishio K, Kanzawa F et al. Synergism between cisplatin and topoisomerase I inhibitors, NB-506 and SN-38, in human small cell lung cancer cells. Cancer Res 1996; 56: 789-793. Lokiec F, Wasserman E, Santoni J et al. Pharmacokinetics PK ; of the irinotecan oxaliplatin LOHP ; combination: preliminary data of an ongoing phase I trial. Proc Soc Clin Oncol 1997; 16: 203a. Benhammouda A, Bastuan G, Rixe O et al. A phase I and pharmacokinetic PK ; study of CPT-11 C ; and 5-FU F ; combination. Proc Soc Clin Oncol 1997; 16: 202a. Rothenberg ML, Pazdur R, Rowinsky EK et al. A phase II multicenter trial of alternating cycles of irinotecan CPT-11 ; and 5-FU LV in patients with previously untreated metastatic colorectal cancer CRC ; . Proc Soc Clin Oncol 1997; 16: 266a. Couteau C, Lokiec F, Vernillet L et al. Phase I dose finding and pharmacokinetic PK ; study of docetaxel D ; in combination with irinotecan I ; in advanced solid tumors. Proc Soc Clin Oncol 1997; 16: 202a. Chabot GG, Abigerges D, Catimel G et al. Population pharmacokinetics and pharmacodynamics of irinotecan CPT-11 ; and active metabolite SN-38 during phase I trials. Ann Oncol 1995; 6: 141-151. Schaaf L, Ichhpurani N, Elfring G et al. Influence of age on the pharmacokinetics of irinotecan CPT-11 ; and its metabolites, SN-38 and SN-38 glucuronide SN-38G ; in patients with previously treated colorectal cancer. Proc Soc Clin Oncol 1997; 16: 202a. Vassal G, Doz F, Lucchi E et al. Phase I trial of irinotecan CPT11 ; in childhood tumors. Proc Soc Clin Oncol 1997; 16: 253a. Herben V, Schellens J, Swart M et al. Phase I and pharmacokinetic PK ; study of irinotecan CPT-11 ; with a prolonged 14D ; infusion schedule. Proc Soc Clin Oncol 1997; 16: 201a. Takaoka K, Ohtsuka K, Jin M et al. Conversion of CPT-11 to its active form, SN-38, by carboxylesterase of non-small cell lung cancer. Proc Soc Clin Oncol 1997; 16: 252a. Chabot GG, Abigerges D, Catimel G et al. Population pharmacokinetics and pharmacodynamics of irinotecan CPT-11 ; and active metabolite SN-38 during phase I trials. Ann Oncol 1995; 6: 141-151. Ohashi N, Fujiwara Y, Yamaoka N et al. No alteration in DNA topoisomerase I gene related to CPT-11 resistance in human lung cancer. Jpn J Cancer Res 1996; 87: 1280-1287. Matsumoto Y, Fujiwara T, Nagao S. Determinants of drug response in camptothecin-11-resistant glioma cell lines. J Neurooncol 1995; 23: 1-8.
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Painful neuropathies are common in people with cancer and may arise from the tumor itself, from treatment of the cancer, or may be totally unrelated to the cancer [1214]. Common cancer-related and noncancer-related neuropathic pain syndromes are listed in Table 1. Of the many etiologies of neuropathies in cancer, chemotherapy-induced neuropathic pain is particularly troublesome, and the use of agents known to produce peripheral neuropathy is increasing. Thus, patients enjoy improved life expectancies, yet reduced quality of life due to significant pain and impaired function. Although many chemotherapeutic agents have been implicated, cisplatin Platinol ; , ifosfamide Ifex ; , paclitaxel, and vincristine in particular are known to consistently cause peripheral neuropathies [15]. In addition, oxaliplatin Eloxatin ; administered parenterally produces an initial, acute, cold allodynia, sometimes within minutes of beginning the infusion. Patients experience this as painful numbness when picking up a cold drink or when they leave the clinic to face cold temperatures. This may be followed by a persistent neuroTHE JOURNAL OF SUPPORTIVE ONCOLOGY.
1 200 fda approval letter for eloxatin oxaliplatin ; , january 9, 200 abstracts articles in support of use of oxaliplatin capecitabine combination in advanced colon and rectal cancer braun ah, achterrath w, wilke h, vanhoefer u, harstrick a, preuss new systemic frontline treatment for metastatic colorectal carcinoma and oxandrolone.
R. Dale Walker, MD, Professor, Departments of Psychiatry and Public Health and Preventive Medicine, Director.
Uwe J Tietge, Rick Havinga, Juul F Baller, Fjodor van der Sluijs, Folkert Kuipers; Groningen Univ Med Cntr, Groningen, The Netherlands The acute phase protein secretory phospholipase A2 sPLA2 ; is a major mediator of decreased plasma HDL cholesterol levels in inflammatory states. The aim of the present study was to investigate the metabolic effects of sPLA2 overexpression in transgenic tg ; mice on biliary and fecal sterol excretion as indicators of reverse cholesterol transport. Compared with controls sPLA2 tg mice had decreased plasma HDL cholesterol levels by 27%, p 0.01 ; and increased in vivo selective uptake of HDL cholesteryl esters into the liver by 38%, p 0.001 ; and the adrenals by 94 %, p 0.001 ; , organs with high expression of SR-BI. Despite increased selective uptake, biliary cholesterol, phospholipid and bile salt secretion as well as fecal bile salt and neutral sterol excretion remained unchanged in sPLA2 tg mice. Livers of sPLA2 tg were significantly larger and enriched in free cholesterol each p 0.001 ; . Consistent with increased cholesterol uptake, hepatic expression of HMG-CoA reductase and the LDL receptor were significantly decreased in livers from sPLA2 tg mice each p 0.001 ; , while expression of SR-BI and ABCG5 G8 were not different between the groups. Hepatic VLDL production in sPLA2 tg was significantly increased p 0.01 ; , whereas the composition of VLDL particles secreted by the liver did not differ between groups. In summary, sPLA2 expression decreases plasma HDL cholesterol levels and increases selective uptake via SR-BI into the liver. However, these changes do not translate into increased biliary and fecal sterol excretion. These data suggest that, in contrast to modulating hepatic SR-BI expression levels, modification of HDL as the ligand for the SR-BI receptor does not impact on reverse cholesterol transport and oxaprozin.
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1. 2. 3. EXECUTIVE SUMMARY THE HIV LIFE CYCLE MUTATIONS AND RESISTANCE NEW GOVERNMENT GUIDELINES HIV AIDS STATISTICS WORLDWIDE ANTIVIRAL DRUGS: NRTIS, NNRTIS, AND PIS 2 4 6 and oxazepam.
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Jeneane burke, msn, mater, thomas jefferson university, philadelphia, pa; kate vandegrift, ma, mater, thomas jefferson university hospital, philadelphia, pa this workshop will focus on barriers and solutions in treating incarcerated opw; the need to partner with all levels of care in providing medically accepted treatment; integrating and developing methods of communication within systems that have individual missions, goals and objectives, and restrictions that present challenges in accomplishing best practice outcomes.
1. Bukowski JF, Warner JF, Dennert G, Welsh RM. Adoptive transfer studies demonstrating the antiviral effect of natural killer cells in vivo. J Exp Med. 1985; 161: 40-52. Uharek L, Zeis M, Glass B, et al. High lytic activity against human leukemia cells after activation of allogeneic NK cells by IL-12 and IL-2. Leukemia. 1996; 10: 1758-1764. Son YI, Dallal RM, Mailliard RB, et al. Interleukin-18 IL-18 ; synergizes with IL-2 to enhance cytotoxicity, interferon-gamma production, and expansion of natural killer cells. Cancer Res. 2001; 61: 884-888. Sedlmayr P, Rabinowich H, Elder EM, et al. Depressed ability of patients with melanoma or renal cell carcinoma to generate adherent lymphokineactivated killer cells. J Immunother. 1991; 10: 336346. Whiteside TL, Vujanovic NL, Herberman RB. Natural killer cells and tumor therapy. Curr Top Microbiol Immunol. 1998; 230: 221-244. Carosella ED, Paul P, Moreau P, Rouas-Freiss N. HLA-G and HLA-E: fundamental and pathophysiological aspects. Immunol Today. 2000; 21: 532534. Raulet DH, Vance RE, McMahon CW. Regulation of the natural killer cell receptor repertoire. Annu Rev Immunol. 2001; 19: 291-330. Maraninchi D, Vey N, Viens P, et al. A phase II study of interleukin-2 in 49 patients with relapsed or refractory acute leukemia. Leuk Lymphoma. 1998; 31: 343-349. Chang E, Rosenberg SA. Patients with melanoma metastases at cutaneous and subcutaneous sites are highly susceptible to interleukin-2based therapy. J Immunother. 2001; 24: 88-90. Mulatero CW, Penson RT, Papamichael D, et al. A phase II study of combined intravenous and subcutaneous interleukin-2 in malignant pleural mesothelioma. Lung Cancer. 2001; 31: 67-72. Benyunes MC, Massumoto C, York A, et al. Interleukin-2 with or without lymphokine-activated killer cells as consolidative immunotherapy after autologous bone marrow transplantation for acute myelogenous leukemia. Bone Marrow Transplant. 1993; 12: 159-163. Hayes RL, Koslow M, Hiesiger EM, et al. Improved long term survival after intracavitary interleukin-2 and lymphokine-activated killer cells for adults with recurrent malignant glioma. Cancer. 1995; 76: 840-852. Fujimiya Y, Suzuki Y, Katakura R, Ohno T. Injury to autologous normal tissues and tumors mediated by lymphokine-activated killer LAK ; cells generated in vitro from peripheral blood mononuclear cells of glioblastoma patients. J Hematother. 1999; 8: 29-37. Kimoto Y, Tanaka T, Tanji Y, Fujiwara A, Taguchi T. Use of human leukocyte antigen-mismatched allogeneic lymphokine-activated killer cells and interleukin-2 in the adoptive immunotherapy of patients with malignancies. Biotherapy. 1994; 8: 4150. Nagayama H, Takahashi S, Takahashi T, et al. IL-2 LAK therapy for refractory acute monoblastic leukemia relapsing after unrelated allogeneic bone marrow transplantation. Bone Marrow Transplant. 1999; 23: 183-185. Rosenberg SA, Lotze MT, Yang JC, et al. Prospective randomized trial of high-dose interleukin-2 alone or in conjunction with lymphokineactivated killer cells for the treatment of patients with advanced cancer. J Natl Cancer Inst. 1993; 85: 622-632. Bergmann L, Schui DK, Brieger J, et al. The inhibition of lymphokine-activated killer cells in acute myeloblastic leukemia is mediated by transforming growth factor-beta 1. Exp Hematol. 1995; 23: 1574-1580. Klingemann HG, Wong E, Maki G. A cytotoxic NK-cell line NK-92 ; for ex vivo purging of leukemia from blood. Biol Blood Marrow Transplant. 1996; 2: 68-75. Yan Y, Steinherz P, Klingemann HG, et al. Antileukemia activity of a natural killer cell line against human leukemias. Clin Cancer Res. 1998; 4: 2859-2868. Tam YK, Miyagawa B, Ho VC, Klingemann HG. Immunotherapy of malignant melanoma in a SCID mouse model using the highly cytotoxic natural killer cell line NK-92. J Hematother. 1999; 8: 281-290. Gong JH, Maki G, Klingemann HG. Characterization of a human cell line NK-92 ; with phenotypical and functional characteristics of activated natural killer cells. Leukemia. 1994; 8: 652-658. Burshtyn DN, Scharenberg AM, Wagtmann N, et al. Recruitment of tyrosine phosphatase HCP by the killer cell inhibitor receptor. Immunity. 1996; 4: 77-85. Tonn T, Becker S, Esser R, Schwabe D, Seifried E. Adoptive cellular immunotherapy of malignancies using the clonal natural killer cell line NK-92. J Hematother Stem Cell Res. 2001; 10: 535-544. Moretta A, Bottino C, Vitale M, et al. Activating receptors and coreceptors involved in human natural killer cell-mediated cytolysis. Annu Rev Immunol. 2001; 19: 197-223. Bach N, Waks T, Eshhar Z. Specific lysis of tumor cells by an NK-like cell line transfected with chimeric receptor genes. Tumor Targeting. 1995; 1: 203-209. Tran AC, Zhang D, Byrn R, Roberts MR. Chimeric zeta-receptors direct human natural killer NK ; effector function to permit killing of NK-resistant tumor cells and HIV-infected T lymphocytes. J Immunol. 1995; 155: 1000-1009. Roberts MR, Cooke KS, Tran AC, et al. Antigenspecific cytolysis by neutrophils and NK cells expressing chimeric immune receptors bearing zeta or gamma signaling domains. J Immunol. 1998; 161: 375-384. Klapper LN, Kirschbaum MH, Sela M, Yarden Y. Biochemical and clinical implications of the ErbB HER signaling network of growth factor receptors. Adv Cancer Res. 2000; 77: 25-79. Olayioye MA, Neve RM, Lane HA, Hynes NE. New EMBO members' review: the ErbB signaling network: receptor heterodimerization in development and cancer. Embo J. 2000; 19: 3159-3167. Wels W, Groner B, Hynes NE. Intervention in receptor tyrosine kinase-mediated pathways: recombinant antibody fusion proteins targeted to ErbB2. Curr Top Microbiol Immunol. 1996; 213: 113-128. Slamon DJ, Leyland-Jones B, Shak S, et al. Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast cancer that overexpresses HER2. N Engl J Med. 2001; 344: 783-792. Wels W, Harwerth IM, Zwickl M, et al. Construction, bacterial expression and characterization of a bifunctional single-chain antibody-phosphatase fusion protein targeted to the human erbB-2 receptor. Biotechnology. 1992; 10: 1128-1132. Stancovski I, Schindler DG, Waks T, et al. Targeting of T lymphocytes to Neu HER2-expressing cells using chimeric single chain Fv receptors. J Immunol. 1993; 151: 6577-6582. Moritz D, Wels W, Mattern J, Groner B. Cytotoxic T lymphocytes with a grafted recognition specificity for ERBB2-expressing tumor cells. Proc Natl Acad Sci U S A. 1994; 91: 4318-4322. Kuwana Y, Asakura Y, Utsunomiya N, et al. Expression of chimeric receptor composed of immunoglobulin-derived V regions and T-cell receptorderived C regions. Biochem Biophys Res Commun. 1987; 149: 960-968. Gross G, Waks T, Eshhar Z. Expression of immunoglobulin-T-cell receptor chimeric molecules as functional receptors with antibody-type specificity. Proc Natl Acad Sci U S A. 1989; 86: 10024-10028. Eshhar Z. Tumor-specific T-bodies: towards clinical application. Cancer Immunol Immunother. 1997; 45: 131-136. Uherek C, Groner B, Wels W. Chimeric antigen receptors for the retargeting of cytotoxic effector cells. J Hematother Stem Cell Res. 2001; 10: 523-534. Altenschmidt U, Kahl R, Moritz D, et al. Cytolysis of tumor cells expressing the Neu erbB-2, erbB-3, and erbB-4 receptors by genetically targeted naive T lymphocytes. Clin Cancer Res. 1996; 2: 1001-1008. Altenschmidt U, Klundt E, Groner B. Adoptive transfer of in vitro-targeted, activated T lymphocytes results in total tumor regression. J Immunol. 1997; 159: 5509-5515. Maurer-Gebhard M, Schmidt M, Azemar M, et al. Systemic treatment with a recombinant erbB-2 receptor-specific tumor toxin efficiently reduces pulmonary metastases in mice injected with genetically modified carcinoma cells. Cancer Res. 1998; 58: 2661-2666. Gerstmayer B, Groner B, Wels W, Schnierle BS. Stable expression of the ecotropic retrovirus receptor in amphotropic packaging cells facilitates the transfer of recombinant vectors and enhances the yield of retroviral particles. J Virol Methods. 1999; 81: 71-75. Evan GI, Lewis GK, Ramsay G, Bishop JM. Isolation of monoclonal antibodies specific for human and oxymorphone.
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Proliferated strongly in vitro against peptide 24962512, and so did a peptide-specific T cell hybridoma, activated with I-Tg-pulsed splenocytes Dai et al., 2002 ; . On the basis of previous observations Duthoit et al., 2000; Dunn et al., 1983 ; , it is possible that mTg fragmentation and the exposure of cryptic epitopes had occurred already during the incorporation of nonphysiological iodine levels into mTg in vitro. All of the above peptides induced peptidespecific antibody responses, but only peptides 25492560 withT4 2553 ; and 24962512 induced the formation of anti-hTg antibodies Kong et al., 1995; Wan et al., 1997; Rasooly et al., 1998; Texier et al., 1992; Chronopoulou and Carayanniotis, 1992 ; . A recent search, conducted by using an algorithm for Ak-binding motifs in mTg, identified five additional immunogenic, non-iodinated and non-dominant epitopes, which induced the proliferation in vitro of peptide-primed, but not mTg-primed, LNCs Table 1 ; . Four of them peptides 306 320, 15791591, and 25962608 ; induced very mild or mild EAT directly, and all induced EAT of low to moderate grade, by the adoptive transfer of peptide-primed LNCs. Peptides 21022116 and 25962608 elicited peptide-specific antibodies that did not react with intact mTg Verginis et al., 2002 ; . Finally, one or more ; non-dominant T-cell epitope s ; was were ; found in peptide 23402359 of hTg, which contained several Ek-binding motifs. This elicited mild to moderate EAT by direct subcutaneous challenge in complete Freund's adjuvant in AKR J mice, and specific proliferative and secretory responses by peptide-primed, but not hTg-primed, LNCs in vitro. Peptide-primed LNCs did not respond to intact hTg, either Karras et al., 2003 ; . Notably, this peptide coincided with a peptide 23392358, TgP15 ; recognized by Tg-reactive B cells in GD patients Thrasyvoulides et al., 2001 ; see Table 1 and Fig. 1 ; . More recently, hTg p2340 has been found able to induce EAT in HLADR3 transgenic mice, suggesting that it could be presented by DR3 molecules in patients with Hashimoto's thyroiditis and participate in the development of the disease Karras et al., 2005 ; . The EAT-causing epitopes of Tg are listed in Table 1, while Figure 1 illustrates their.
| Oxaliplatin onlineMaterials and Methods Brains with cerebral aneurysm were collected between 1976 and 1982 from the departments of pathology of Kyoto University School of Medicine, Shiga University of Medical Science and Fukui Red Cross Hospital. The circles of Willis were carefully separated from the brains fixed in 10% formalin. Absent parts of the incomplete circles were considered as torn and as such were not taken into account. We studied 44 cases of completely preserved circles of Willis. Variations and aneurysm sites were examined macroscopically as well as under magnification. Sketches were made afterwards. A series of 148 circles of Willis without aneurysm from Kyoto University served as the control.3 The "typical" circle of Willis was defined with respect to its components as a closed circuit in which fluid may circulate from any entrance point back to the same point with all vessels more than 1 mm in external diameter and with no excess vessels. Paired vessels were considered asymmetrical if the thicker was at least twice the size of the thinner one regardless of their respective size. Variations were classified according to Ozaki's classification, 3 which we slightly modified as follows fig. 1 ; : 1 ; Fenestration of the anterior communicating artery including V-, Y-, H-, and N-shaped, double and oxytocin.
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Prognosis patient: its median survival on 5-FU could be over 24 months, on Oxaliplatin again over 24 months and this patient would have a good chance of having a therapeutic response to CPT-11 without excessive toxicity. On the other hand a patient whose tumor has a low TS content and a high DPD content, homozygous for the Isoleucin Isoleucin phenotype would have a poor chance of response to 5-FU and shall be probably resistant to Oxaliplatin. If this patient is in addition either homozygous to UGT1-A1- 28 he would have a significant risk for severe toxicity on CPT-11. This patient would be a classical poor prognosis patient even with the most recent drugs. REFERENCES.
Thirty-five patients with heavily pretreated or cisplatinrefractory nonseminomatous germ cell cancer were entered onto the study between August 2001 and March 2003. Patient characteristics at the time of inclusion onto this study are listed in Table 1; 13 patients 37% ; had liver metastases and five patients 14% ; had brain involvement. All patients were heavily pretreated with a median number of six range, four to 13 ; cisplatin-containing chemotherapy cycles before gemcitabine plus oxaliplatin therapy, and 31 patients 89% ; had previously received carboplatin plus etoposidebased high-dose chemotherapy with autologous stem-cell support. Nineteen of 31 patients 61% ; had undergone at least two high-dose chemotherapy cycles. Twenty-two and paclitaxel.
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Next, mentally take that given flaw with you to the theatre this week when you go to see Mel Gibson's movie The Passion. Then as you watch what happens to Christ, tell yourself, "My anger, or my greed, my lust, my sloth, my gluttony, my envy, my pride, is partly responsible for what he's having to suffer. God is laying my iniquity on his son and oxaliplatin.
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References 1. 2. 3. Raymond E, Chaney SG, Taamma A, Cvitkovic E. Oxaliplatin: a review of preclinical and clinical studies. Ann Oncol 1998; 9: 1053 Bleiberg H. Oxaliplatin: a new reality in colorectal cancer. Br J Cancer 1988; 77: Suppl. 4, 1 3. Extra JM, Marty M, Brienza S, Misset JL. Pharmacokinetics and safety profile of oxaliplatin. Semin Oncol 1998; 25: 13 Misset JL. Oxaliplatin in practice. Br J Cancer 1998; 77: Suppl. 4, 7. Lee KS, Kim Y, Han J, Ko EJ, Park CK, Primack SL. Bronchioloalveolar carcinoma: histopathologic, and radiologic findings. Radiographics 1997; 17: 1345 McCulloch GL, Sinnatamby R, Stewart S, Goddard M, Flower CD. High-resolution computed tomographic appearance of MALToma of the lung. Eur Radiol 1998; 8: 1669 Nagakawa T. CT of metastatic pulmonary tumors: morphology, HRCT and histological correlation. Nippon Igaku Gakka Zasshi 1996; 56: 1032 Gaeta M, Volta S, Scribano E, Loria G, Vallone A, Pandolfo I. Air-space pattern in the lung metastasis from adenocarcinoma of the GI tract. J Comput Assist Tomogr 1996; 20: 300 Myers J. Pathology of drug-induced lung disease. In: Katzenstein ed ; Katzenstein and Askin9s Surgical Pathology of Non-Neoplastic Lung Disease. Philadelphia, WB Saunders, 1997; pp. 81 111. Monnet I, Brienza S, Hugret F, et al. Phase II study of oxaliplatin in poor-prognosis non-small cell lung cancer NSCLC ; . Eur J Cancer 1998; 34: 1124 Jeanfaivre T, Saint-Andre JP, Laine P, Tuchais E. ` ` Fibrose pulmonaire aigue au decors d9un traitement par fluorouracile et cisplatine. Therapie 1995; 50: 167 Fielding JWL, Stockley RA, Brookes VS. Interstitial lung disease in a patient treated with 5-fluorouracil and mitomycin C. BMJ 1978; ii: 602. Fielding JWL, Stockley RA, Brookes VS. Interstitial fibrosis in a patient treated with 5-fluorouracil and mitomycin C. BMJ 1979; ii: 551 552.
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North Herts & Stevenage Primary Care Trust pharmaceutical development group evening meeting on the new pharmacy contract, Novotel Hotel, Stevenage, 7 June.This meeting is open only to community pharmacists, including locums, working in the PCT area. Further information from Mike Beaman and oxandrolone.
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