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Posted: tue may 31, 2005 2: post subject: illness can make pigs irritable and more contentious with their cagemates. CAP18106-138 -IgG, a construct that, in concentrations equimolar to those of peptide alone, binds and neutralizes LPS and kills multiple gram-negative bacterial strains. The protective efficacy of CAP18106-138 -IgG was evaluated in a model of cecal ligation and puncture in mice. A single intravenous administration of 20 mg kg CAP18 106-138 -IgG protected against mortality, compared with sham-coupled IgG P .03 ; . There was no protection offered by administration of equimolar peptide alone P .96 ; . There was a trend toward protection in C3H HeJ mice that are minimally sensitive to LPS P .06 ; , suggesting that direct detoxification of LPS was not the only mechanism of protection. Chemical or genetic coupling of antimicrobial peptides to IgG may be a means of using these peptides to treat infections. 597. Association of Mannose-Binding Lectin Polymorphisms with Sepsis and Fatal Outcome, in Patients with Systemic Inflammatory Response Syndrome - Garred P., Strm J.J., Quist L. et al. [Dr. P. Garred, Tissue Typing Laboratory-7631, Dept. of Clinical Immunology, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen , Denmark] - J. INFECT. DIS. 2003 188 9 ; summ in ENGL Genetic factors may predispose critically ill patients to increased risk of developing sepsis. Mannose-binding lectin MBL ; is an important factor in innate immune defense. We investigated whether MBL gene polymorphisms causing low levels of MBL are associated with the development and progression of sepsis in adult patients in intensive care units. In 272 prospectively monitored patients with systemic inflammatory response syndrome, different MBL genotypes were compared, with respect to microbiology, sepsis development, and survival. The presence of MBL variant alleles was associated with the development of sepsis, severe sepsis, and septic shock. An increased risk of fatal outcome was observed in patients carrying variant alleles. These data show that MBL insufficiency plays an important role in the susceptibility of critically ill patients to the development and progression of sepsis and confers a substantial risk of fatal outcome. 598. Geranylgeranylacetone attenuates septic diaphragm dysfunction by induction of heat shock protein 70 - Masuda Y., Sumita S., Fujimura N. and Namiki A. [Dr. Y. Masuda, Department of Anesthesiology, Sapporo Med. Univ. Sch. of Medicine, West-16, South-1, Chuo-ku, Sapporo, Hokkaido, 060-8543, Japan] - CRIT. CARE MED. 2003 31 11 ; - summ in ENGL Objective: The purposes of the present study were to evaluate the induction of heat shock protein HSP ; 70 expression in the diaphragm by geranylgeranylacetone GGA ; administration and to determine the effect of HSP70 induction on diaphragm contractility measured in vitro and the production of oxygen-derived free radicals during experimental septic peritonitis. Design: Prospective laboratory study. Setting: University laboratory. Subjects: Onehundred sixty male Wistar rats. Interventions: In experiment 1, rats received GGA intragastrically, and time-dependent induction of HSP70 expression in the diaphragm was determined at 0, 12, 24, and 36 hrs after GGA administration. To evaluate dose-dependent inhibition of GGA-induced HSP70 expression by quercetin, rats were pretreated with progressive doses of quercetin before GGA administration. In experiment 2, rats received gum arabic solution vehicle ; , 100, 200, or 400 mg kg of GGA. In experiment 3, rats were pretreated with quercetin or glycerol before GGA or vehicle administration. Intra-abdominal sepsis was induced by cecal ligation and perforation CLP ; under inhalation anesthesia after GGA or vehicle administration in experiments 2 and 3. Measurements and Main Results: Western blot analysis using diaphragm homogenates obtained from normal rats showed that HSP70 expression peaked at 24 or hrs after GGA administration and that pretreatment with 10 mg kg of quercetin blocked the induction of HSP70 expression by GGA. CLP induced diaphragmatic dysfunction and increased diaphragmatic malondialdehyde concentrations and superoxide dismutase and glutathione peroxidase activities. GGA attenuated CLP-induced diaphragm dysfunction and increased malondialdehyde concentrations in a dose-dependent manner but did not affect superoxide dismutase and glutathione peroxidase activities after CLP. Diaphragm dysfunction and increased diaphragmatic malondialdehyde concentrations after CLP were maintained on quercetin pretreatment despite GGA administration. Conclusions: 121, for instance, drug information.

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A: unlike bypass surgery, balloon angioplasty, and stenting procedures, eecp is non-invasive, carries no risk, is comfortable, and is administered in outpatient sessions. 111-AM Segment Identification 8 DUR PPS Segment. 473-7E DUR Code Counter Counter number for each DUR PPS set logic grouping. 439-E4 Reason for Service Code Code identifying the type of utilization conflict detected or the reason for the pharmacist's professional service. DD Drug-Drug Interaction HD High Dose ID Ingredient Duplication TD Therapeutic 44-E5 Professional Service Code Code identifying pharmacist intervention when a conflict code has been identified or service has been rendered. No Intervention M Prescriber consulted P Patient consulted and bisoprolol. Quantitative pcr analysis indicated up regulation of hif-1 α in casodex treated lncap-r and lncap-ur cells figure 2 , panel b.

10 ; Anonymous. 1995 The Year in Review. Drug Store New For The Pharrnacistl996; 6 4 ; . 11 ; Conlin ME NY Report Decries Rx Drug Switching by PBMs. Drug Topics 1997; 141 2 and zebeta, for instance, nilutamide.
The impairment must result in substantial adverse effect, so mild arthritis or simple forgetfulness may not be enough. Remember that the Act requires the impairment to have a substantial adverse effect on the person's ability to carry out normal day to day activities. A person who finds it convenient to have medicines dispensed in a monitored dosage system or a person who wants tablets popped out of blister packs because of a preference for glass screw top bottles is not necessarily disabled.

CASODEX is indicated for use in combination therapy with a luteinizing hormone-releasing hormone analog LHRH-A ; for the treatment of Stage D2 metastatic carcinoma of the prostate. CASODEX 50 mg qd plus an LHRH-A was not significantly different from flutamide 250 mg tid plus an LHRH-A for time to progression and survival.1, 2 and bupropion. The doctor put me on inhaler medicine.

Seeming such interventions would have to be culturally competent. Without representation of diversity on the health care team, it is conceivable that minimal participation and reluctance to under take meaningful lifestyle changes thereby affecting outcomes might occur among vulnerable ethnic minority populations and isoptin.

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13. Zirvi KA, Keogh JP, Slomiany A and Slomiany BL: Transglutaminase activity in human colorectal carcinomas of differing metastatic potential. Cancer Lett 60: 85-92, 1991. Mignatti P and Rifkin DB: Biology and biochemistry of proteinases in tumor invasion. Physiol Rev 73: 161-195, 1993. Blasi F and Stoppelli MP: Proteases and cancer invasion: from belief to certainty. AACR meeting on proteases and protease inhibitors in cancer, Nyborg, Denmark, 14-18 June 1998. Biochim Biophys Acta 1423: R35-R44, 1998. 16. Matrisian LM: Cancer biology: extracellular proteinases in malignancy. Curr Biol 9: 776-778, 1999. Witty JP, McDonnell S, Newell KJ, Cannon P, Navre M, Tressler RJ and Matrisian LM Modulation of matrilysin levels in colon carcinoma cell lines affects tumorigenicity in vivo. Cancer Res 54: 4805-4812, 1994. Masaki T, Matsuoka H, Sugiyama M, Abe N, Goto A, Sakamoto A and Atomi Y: Matrilysin MMP-7 ; as a significant determinant of malignant potential of early invasive colorectal carcinomas. Br J Cancer 84: 1317-1321, 2001. Andreasen PA, Egelund R and Petersen HH: The plasminogen activation system in tumor growth, invasion, and metastasis. Cell Mol Life Sci 57: 25-40, 2000. Berger DH: Plasmin plasminogen system in colorectal cancer. World J Surg 26: 767-771, 2002. Sordat BC and Tran-Thang C: Laminin degradation by human colon carcinoma cells: a role for urinary and tissue plasminogen activators. Invasion Metastasis 14: 223-233, 1994. Weitz JI, Stewart JR and Fredenburgh JC: Mechanism of action of plasminogen activators. Thromb Haemost 82: 974-982, 1999. Shah V, Kumar S and Zirvi KA: Metastasis of human colon tumor cells in vivo: correlation with the overexpression of plasminogen activators and 72 kDa gelatinase. In vivo 8: 321-326, 1994. Leibovitz A, Stinson JC, McCombs WB III, McCoy CE, Mazur KC and Mabry ND: Classification of human colorectal adenocarcinoma cell lines. Cancer Res 36: 4562-4569, 1976. Skehan P, Storeng R, Scudiero D, Mons A, McMahon J, Vistica D, Warren JT, Boekesch H, Kenney S and Boyd MR: New colorimetric cytotoxicity assay for anti-cancer drug screening. J Natl Cancer Inst 82: 1107-1112, 1990. Jones LJ, Gray M, Yue ST, Haugland RP and Singer VL: Sensitive determination of cell number using CyQUANT cell proliferation assay. J Immunol Methods 254: 185-198, 2001. Lowry OG, Rosebrough NJ, Farr AL and Randall RJ: Protein measurements with the Folin phenol reagent. J Biol Chem 193: 265-275, 1951. Wang LG, Liu XM; Kreis W and Budman DR: The effect of antimicrotubule agents on signal pathways of apoptosis: a review. Cancer Chemother Pharmacol 44: 355-361, 1999. Sciola L, Spano A, Monaco G, Bottone MG and Barni S: Different apoptotic responses and patterns in adhering and floating neoplastic cell cultures: effect of microtubule antagonists. Histochem Cell Biol 119: 77-90, 2003. Satya-Prakash KL, Hsu TC and Wheeler WJ: Metaphase arrest, anaphase recovery and aneuploidy induction in cultured Chinese hamster cells following exposure to mitotic arrestants. Anticancer Res 4: 151-156, 1984. Jordan MA, Wendell K, Gardiner S, Derry WB, Copp H and Wilson L: Mitotic block induced in HeLa cells by low concentrations of paclitaxel Taxol ; results in abnormal mitotic exit and apoptotic cell death. Cancer Res 56: 816-825, 1996. Andreassen PR, Martineau SR and Margolis RL: Chemical induction of mitotic checkpoint override in mammalian cells results in aneuploidy following transient tetraploid state. Mutat Res 372: 181-194, 1996. Mareel MM and De Mets M: Effect of microtubule inhibitors on invasion and related activities of tumor cells. Int Rev Cytol 90: 125-168, 1984. Stearns ME and Wang M: Taxol blocks processes essential for prostate tumor cell PC-3 ML ; invasion and metastases. Cancer Res 52: 13776-13781, 1992. Zhan P, Lee EC, Packman K and Tenniswood M: Induction of invasive phenotype by Cxsodex in hormone-sensitive prostate cancer cells. J Steroid Biochem Mol Biol 83: 101-111, 2002 and captopril.
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CASODEX bicalutamide ; Tablets disability, overall health, physical capacity, general symptoms, and treatment related symptoms. Assessment of the Quality of Life questionnaires did not indicate consistent significant differences between the two treatment groups. Safety Data from Clinical Studies using CASODEX 150 mg CASODEX 150 mg is not approved for use either alone or with other treatments. Two identical multicenter, randomized, open label trials comparing CASODEX 150 mg daily monotherapy to castration were conducted in patients that had locally advanced T3-4, NX, MO ; or metastatic M1 ; prostate cancer. Monotherapy M1 Group CASODEX 150 mg daily is not approved for use in patients with M1 cancer of the prostate. Based on an interim analysis of the two trials for survival, the Data Safety Monitoring Board recommended that CASODEX treatment be discontinued in the M1 patients because the risk of death was 25% HR 1.25, 95% CI 0.87 to 1.81 ; and 31% HR 1.31, 95% CI 0.97 to 1.77 ; higher in the CASODEX-treated group compared to that in the castrated group, respectively. Locally Advanced T3-4, NX, MO ; Group CASODEX 150 mg daily is not approved for use in patients with locally advanced T3-4, NX, M0 ; cancer of the prostate. Following discontinuation of all M1 patients, the trials continued with the T3-4, NX, MO patients until study completion. In the larger trial N 352 ; , the risk of death was 25% HR 1.25, 95% CI 0.92 to 1.71 ; higher in the CASODEX group and in the smaller trial N 140 ; , the risk of death was 36% HR 0.64, 95% CI, 0.39 to 1.03 ; lower in the CASODEX group. In addition to the above two studies, there are three other on-going clinical studies that provide additional safety information for CASODEX 150 mg, a dose that is not approved for use. These are three multicenter, randomized, doubleblind, parallel group trials comparing CASODEX 150 mg daily monotherapy adjuvant to previous therapy or under watchful waiting ; with placebo, for death or time to disease progression, in a population of 8113 patients with localized or locally advanced prostate cancer. CASODEX 150 mg daily is not approved for use as therapy for patients with localized prostate cancer who are candidates for watchful waiting. Data from a planned subgroup analysis of two of these trials in 1, 627 patients with localized prostate cancer who were under watchful waiting, revealed a trend toward decreased survival in the CASODEX arm after a median follow-up of 7.4 years. There were 294 37.7% ; deaths in the CASODEX treated patients versus 279 32.9% ; deaths in the placebo treated patients localized watchful waiting group ; for a hazard ratio of 1.16 95% CI 0.99 to 1.37 ; . INDICATIONS AND USAGE CASODEX 50 mg daily is indicated for use in combination therapy with a luteinizing hormone-releasing hormone LHRH ; analogue for the treatment of Stage D2 metastatic carcinoma of the prostate. CASODEX 150 mg daily is not approved for use alone or with other treatments. See CLINICAL PHARMACOLOGY - Clinical Studies - Safety Data from Clinical Studies using CASODEX 150 mg section for additional important safety information regarding CASODEX 150 mg. CONTRAINDICATIONS.
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LOCATION: Teleconference 1-800-315-6338 THA Members present: Carol White, Justine Muench, Judy Neary, Matthew Schnellbaecher, Teresa Ferguson, Kathy Boulton, Beth Helgunson, Tzu-Ching, Liu, Pam Borg-Jensen, Kristin Wurz, Sharon Stiassney Members absent: 10 Guests: 0 Minutes: Debra L. Stevens ITEM Review of MI ACS Diagnosis, Discharge Orders and QA Checklist DISCUSSION Group discussion on MI Order Sets. Starting with the Diagnosis Admission. This is the list that we came up with based on four or five different orders sets. The group decided that we wanted just one page and hospitals would add specific orders for drugs that have dosing charts. This is a template to get people jump started and orders that match CMS indicators. Dr. Schnellbaecher suggested that the Acute ST Elevated MI Orders should be a whole different pathway. Treatments: Dr. Schnellbaecher suggested that we add a check box for Iodine allergies because a lot of these people are going to be getting catheterized so it's kind of a prompt for the staff to ask. No other suggestions. Diagnostics: Justine asked the group if she should separate out the chest x-ray? Justine asked or suggested that maybe there should be separate boxes, so it would be a box for CBC, a box for CMP. Lipid should be clarified on admission and NPO. Next, Justine asked if anyone had any suggestions regarding the EKG and the Echocardiogram lines. Dr. Schnellbacher said on their form under Echocardiogram they write "chest pain, evaluate wall motion" since the clerks sitting at the desk needs to know what to put in that line. It was suggested that the Date required line be removed. Activity: Nutrition Hydration: Dr. Schnellbacher suggested that he would have a check box for the IV; what type of IV at per-hour. Medications: Dr. Schnellbacher said that it would be nice to put the amount of dosage like medium to high dosage of a moderate to potent statin. Dr. Schnellbaecher explained that we should keep the order sets to one page Take out Metabolic Profile ACTION FOLLOW-UP Orders should be on one page.

J hepatol 1994; 7-672 stanley mm, ochi s, lee kk, nemchausky ba, greenlee hb, allen ji, et al peritoneovenous shunting as compared with medical treatment in patients with alcoholic cirrhosis and massive ascites and catapres and casodex, because antiandrogen.

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Commonly referred to as acid, a hit or dose can be found as tablets, capsules, clear liquid, thin squares of gelatin, or colorful paper dipped in lsd that is licked. The plasma of the tumored animals was analyzed by HPLC. Plasma was treated enzymatically with glucuronidase sulfatase to recover native quercetin. Quercetin was identified in the treated animals. Taken together, these results indicate quercetin decreases cellular GSH levels and sensitizes cells to apoptosis. The effects can be increased by tumor-like low pH. Dietary quercetin resulted in a tumor growth delay, and blood levels in the range needed for radio radiosensitization can be achieved. Studies are now underway to demonstrate radiosensitization by quercetin in vitro and in vivo. In addition this project has resulted in the submission of a grant to the American Institute for Cancer Research entitled "Tumor Radiosensitization by Dietary Quercetin." Project Title: Improvement of tumor control by combining a VEGF blocker, VEGF Trap with Radiation Therapy. Collaborators: Pharmaceutical Industry, Regeneron Pharmaceuticals Tarrytown, NY ; and Phyllis Wachsberger, Thomas Jefferson University, Philadelphia PA. Novel Drug: VEGF Trap. We have established collaboration between the core, Regeneron Pharmaceuticals, and Dr. Phyllis Wachsberger, an Assistant Professor at Thomas Jefferson University, to study a novel VEGF Trap that has great potential to be used in combination with radiation therapy. This project can be translated quickly into the clinic. Dr. Wachsberger is the primary investigator of the project and works with the core. Recent preclinical studies have suggested that radiotherapy in combination with vascular endothelial growth factor VEGF ; targeting agents can enhance the therapeutic ratio of ionizing radiation by targeting both tumor cells and tumor vessels. VEGF Trap is a soluble decoy VEGF receptor, which can selectively inhibit the activity of VEGF, a growth factor influencing the high levels of vascularization and growth in many tumors. The objective of the present study was to evaluate the effect of VEGF Trap from Regeneron ; on tumor growth delay TGD ; in response to ionizing radiation in the clinically relevant U87 human gliobastoma model, which is known to express high levels of VEGF. U-87 VEGF Trap was used at two doses, high 25mg kg ; and low 2.5 mg kg ; , given every three days for up to three weeks, using the same schedule with and without a single dose of radiation of 10 Gy. Control tumors had an average TGD of 10 days whereas low dose VEGF Trap increased TGD an additional 10 days. A single dose of radiation of 10 Gy increased TGD 10 days over that of control whereas radiation plus low dose VEGF Trap increased TGD 20-25 days over that of control. High dose VEGF Trap increased TGD 40 days over that of control but did not show any increased benefit when combined with radiation. It is concluded that VEGF Trap alone is an effective inhibitor of tumor growth in the U87 gliobastoma model and that low dose VEGF Trap in combination with single dose radiation has an enhanced effect on tumor cell kill. This study suggests that VEGF Trap may be of benefit in a fractionated radiotherapy regimen. Regeneron will provide continued funding for this project. In addition a Phase 1 clinical trial is planed using radiation therapy in the RTOG. Therefore, this project is an example of how the NDDPC can work with the pharmaceutical industry to generate and cefaclor. For 25 respondents 47, 2 % ; , cephalosporins is a critically important family of antimicrobials. It seems that the use of cephalosporins in veterinary medicine is limited in Africa. 4.4.4. Use of cephalosporins in veterinary medicine Cephalosporins are used to treat a wide range of medically and economically important animal diseases. Treatment with cephalosporins is of individual animals, either by parenteral, oral or local routes for the latter e.g. mastitis ; . Oral treatment of groups of food animals is not approved. Table 5 and graphic 14: The importance of cephalosporins by species and for some diseases.

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Because of significant costs and a lack of specific FDA indications, managed care plans have had to develop policies on the use of agents for CDH.57 These policies seek to achieve optimal clinical outcomes while maintaining cost effectiveness and minimizing medical-legal risk. 3 to 16 days ; pharmacy q: whether the casdoex prescription is required for buying this medicine. Castration cazodex 100 mg casodex 150 mg 18 49 45 not significant and bisoprolol. What are your views on medicinal marijuana, or medicinal cocaine. When selecting over-the-counter pain medication, you are now faced with choices that you didn't have, even a few years ago. But not all pain pills are the same. Which one you choose should depend on the situation. These different cell subpopulation requirements for the generation of antigen-specific cellular responses seem to be dependent on the model, the characteristics of the antigen, and its level of surface expression on APCs, as well as the immunization method. The mechanism of CD4-mediated help when immunizing with genetically modified DCs had not been reported before this study. When immunizing with DCs genetically modified to express two different tumor antigens MART-1 and AFP ; , we have reported previously that CD4 T cells are required to generate protective immunity 8, 33 ; . In these models, the response is mediated by a MHC class I-restricted cellular cytotoxic response 1, 8 ; and is generated directly by the immunizing gene-modified DCs and not by cross-priming through host APCs 9 ; . These data suggest that adenovirus-mediated endogenous expression of a foreign antigen into DCs leads to epitope presentation through both MHC class I and II. In the current studies, we attempted to determine the role and pathway involved in the CD4 T-cell function when mice are immunized with tumor antigen genemodified syngeneic DCs. Our data strongly support the notion that CD4 T cells are helper cells in this model, which engage the CD40mediated pathway. This helper function cannot be substituted by the supraphysiological production of the type 1 cytokines IL-2, IL-7, or IL-12 when the DCs are transduced with viral vectors expressing levels of these cytokines that are much higher than in CD40-crosslinked DCs. CD40 engagement in the DCs used for immunization leads to detectable changes in cell surface expression of MHC and costimulatory molecules, which may mediate an enhanced ability to stimulate naive MART-1-specific T cells in the host 34 ; . A consistent finding in our studies is an unexpected high rate of antitumor protection in CD4KO mice immunized with CD40-crosslinked DCs. In four of seven studies, this was superior to AdVMART1 DC immunization in wild-type mice, although this trend was not statistically significant. This trend toward greater protection was not correlated with greater in vitro cytotoxic activity or type 1 cytokine production in most studies, lysis in 51Cr release assays and number of IFN producing cells in ELISPOT assays was higher in wild-type mice compared with CD4KO mice immunized with CD40cross-linked DCs ; . Recent data suggest that CD4 T cells not only provide help to CD8 T-cell activation but also enhance the ability of effector cells to infiltrate tumors and are responsible for maintaining. With 0 0-thalassemia and co-inheritance of a single -globin gene deletion all showed the -thalassemia major phenotype, while 0 + -thalassemia and co-inheritance of a single -globin gene deletion, observed in only one patient, was associated with a -thalassemia intermedia phenotype. Our results show that co-inheritance of the SEA deletion ameliorates the clinical phenotype of 0 + but not necessarily that of 0 0-thalassemia in Chinese patients with severe -thalassemia. However, no definite conclusion is warranted about the phenotypic effect of a single -globin gene deletion in view of the many fewer cases than the SEA deletion. This conclusion has two clinical implications. First, we propose that the presence of SEA deletion should be routinely determined in couples at risk of conceiving a fetus affected by 0 + -thalassemia i.e. parents who are discordant carriers of 0- and + -thalassemia mutations ; , so that this information may be incorporated into the genetic counseling of such couples. Based on prevalence figures of -thalassemia alleles10 and assuming 70, 000 live births annually, this amounts to eight pregnancies 0.004 0.027 70, 000 ; per year. As Hb H inclusion bodies are typically absent in subjects who are heterozygous for both -thalassemia mutation and SEA deletion, the presence of SEA deletion must be detected by PCRbased techniques.10 Second, at prenatal diagnosis, a genotype of 0 + -thalassemia and SEA deletion for the fetus is predictive of -thalassemia intermedia, whereas the same cannot be said for compound heterozygous 0 + -thalassemia only or 0 0-thalassemia in association with SEA deletion. Edmond Shiu Kwan Ma, * Amy Yuk Yin Chan, * Sau Yin Ha, Godfrey Chi Fung Chan, Wing Yan Au, # Li Chong Chan * Departments of * Pathology, Pediatrics and #Medicine, The University of Hong Kong, Queen Mary Hospital; Hong Kong, People's Republic of China Key words: SEA deletion, -thalassemia, -thalassemia, thalassemia intermedia, genotype-phenotype correlation. Correspondence: Dr. Edmond Shiu Kwan Ma, Division of Hematology, Department of Pathology, The University of Hong Kong, Queen Mary Hospital, 102 Pokfulam Road, Hong Kong, People's Republic of China. Phone: international + 852.28554570. Fax: international + 852.28177565. E-mail: eskma hkucc.hku.hk.

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