Antibodies treatment

Premature Ventricular Depolarixation No PbTx Antibody Treatment (Lead VIO. 1 cm/mv. 25 mm/sec)... 

Herdon, F.J. and Kayes, S.G. (1992) Depletion of eosinophils by anti-IL-5 monoclonal antibody treatment of mice infected with Trichinella spiralis does not alter parasite burden or immunologic resistance to re-infection. Journal of Immunology 149, 3642-3647. 

Papadopoulos, C. M., Tsai, S-Y., Alsbiei, T., O Brien, T. E., Schwab, M. E. and Kartje, G. L. Functional recovery and neuroanatomical plasticity following middle cerebral artery occlusion and IN-1 antibody treatment in the adult rat. Ann. Neurol. 51 433-441, 2002. 

Emmrich, J. et al., Anti-CD6 antibody treatment in inflammatory bowel disease without along CD4+-celldepletion [abstract], Gastroenterology, 108, 146, 1995. 

You S, Leforban B, Garcia C, Bach JF, Bluestone JA, Chatenoud L Adaptive TGF-p-dependent regulatory T cells control autoimmune diabetes and are a privileged target of anti-CD3 antibody treatment. Proc Natl Acad Sd USA 2007 104 6335-6340. 

The advent of recombinant DNA technology led to the development of antibodies and fragments that are tailored for optimal behaviour in vivo [7,8]. Humanized and chimeric antibodies can be constructed to circumvent the human anti-mouse antibody response elicited by mouse antibody treatment of patients, which severely hampers the application of these powerful molecules. The treatment of rheumatoid arthritis patients with doses of as high as 10 mg kg cA2 chimeric antibody specific for TNFa [9], emphasizes that at present the production and purification methods for these proteins have been optimized to such extent that clinical studies can be considerably intensified. 

Embrel (Immunex) Monoclonal antibody (treatment of rheumatoid arthritis) 0.7... 

Murry, J. (2000). Monoclonal antibody treatment of solid tumors a coming of age. Semin. Oncol. 27(6), 64-70. Senter, P. Springer, C. (2001). Selective activation of anticancer prodrugs by monoclonal antibody-enzyme conjugates. Adv. Drug Deliv. Rev. 53(3), 247-264. 

IX.b.3.4. Genetically engineered antibodies. Anti-TNF antibody treatment with infliximab or adalimumab is now accepted as of value in treating severe and fistulating exacerbations of Crohn s disease when standard treatments are not tolerated or have failed. Adverse effects which limit usefulness include the occurrence of tuberculosis and septicaemia, leucopenia and pancytopenia, and risk of exacerbation of demyelinating disease. Considerations of benefits versus risks of such treatment are complex, but probably positive. 

Arnason BG Long-term experience with interferon beta-lb (Betaferon) in multiple sclerosis. J Neurol 2005 252(Suppl 3) iii28. Brown MA Antibody treatments of inflammatory arthritis. Curr Med Chem 2005 12 2943. [PMID 16378497]... 

Braendstrup P, Bjerrum OW, Nielsen OJ, Jensen BA, et al. 2005. Rituximab chimeric anti-CD20 monoclonal antibody treatment for adult refractory idiopathic thrombocytopenic purpura. Am... 

Zheng XX, Markees TG, Hancock WW, Li Y, et al. 1999. CTLA4 signals are required to optimally induce allograft tolerance with combined donor specific transfusion and anti-CD154 monoclonal antibody treatment. J Immunol. 162 4983-4990. 

Coles AJ, Wing M, Smith S, Coraddu F, Greer S, Taylor C, Weetman A, Hale G, Chatteqee VK, Waldmann H, Compston A. Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis. Lancet 1999 354(9191) 1691-5. 

Murray, J. L. 2000. Monoclonal antibody treatment of solid tumors. Sem. Oncol. 27 64—70. 

Therapeutic monoclonal antibodies are widely recognized to be a most promising means to treat an increasing number of human diseases, including cancers and autoimmunity. To a large extent, the efficacy of monoclonal antibody treatment is because IgG antibodies have greatly extended persistence in vivo. However, conventional rodent models do not mirror human antibody pharmacokinetics. The key molecule responsible for the extended persistence antibodies is the major histocompatibility complex class I family Fc receptor, FcRn. We describe human FcRn transgenic mouse models and how they can be exploited productively for the preclinical pharmacokinetic evaluation of therapeutic antibodies. 

Railed, S. L., A. H. Cutler, S. K. Datta, and D. W. Thomas. 1998. Anti-CD40 ligand antibody treatment of SNF1 mice with established nephritis preservation of kidney function. J. Immunol. 160 2158-2165. 

Tak, P. P., Taylor, P. C., Breedveld, F. C., Smeets, T.J., Daha, M. R., Kluin, P. M. etal. (1996). Decrease in cellularity and expression of adhesion molecules by anti-tumor necrosis factor a monoclonal antibody treatment in patients with rheumatoid arthritis. Arthritis Rheum. 39, 1077-1081. 

Early, G. C., Laman, J. D., Zhao, W., Noelle, R. J., and Burns, C. M. Anti-CD40 ligand antibody treatment of NZB/NZW mice prevents the development of lupus-like nephritis without generating an antibody response in responding mice. 

Park, J. W., Kirpotin, D., Shalaby, R., Hong, K, Shao, Y., Marks, J., Papahadjopoulos, D., and Benz, C. C. (1998). Anti-HER2 immunoliposomes Significantly superior efficacy vs. doxorubicin, liposomal doxorubicin, and anti-her2 antibody treatment, via novel mechanism of action. Proc. Am. Soc. Clin. Oncol. 17, 216a. 

Skvortsov S, Sarg B, Loeffler-Ragg J, Skvortsova I, Lindner H, Werner Ott H, et al. Different proteome pattern of epidermal growth factor receptor-positive colorectal cancer cell lines that are responsive and nonresponsive to C225 antibody treatment. Mol Cancer Ther 2004 3(12) 1551-1558. 

The arterial and venous catheters are placed surgically under aseptic conditions. These catheters are used for hemodynamic monitoring, fluid and antibody treatments, and blood sampling. 

Cheng G, Arima M, Honda K, Hirata H, Eda F, Yoshida N, Fukushima F, Ishii Y, Fukuda T. Anti-interleukin-9 antibody treatment inhibits airway inflammation and hyperreactivity in mouse asthma model. Am. J. Respir. Crit. Care. Med. 2002 166 409 16. 

Delmonico, F.L. Cosimi, A.B. Monoclonal antibody treatment of human allograft recipients. Surg. Gynecol. Obstet. 1988, 166, 89-98. 

Cavalli-Bjorkman N, Osby E, Lundin J, Kalin M, Osterborg A, Gruber A. Fatal adenovirus infection during alemtuzumab (anti-CD52 monoclonal antibody) treatment of a patient with fludarabine-refractory B cell chronic lymphocytic leukemia. Med Oncol 2002 19(4) 277-80. 

Inhibitors of factor VIII are the most common and develop in 5-15% of patients with hemophilia A. Inhibitors of factor IX develop in 1 % of patients with hemophilia B (11,12). Patients with hemophiha B with complete gene deletions or derangement of the factor IX gene are particularly at risk of developing antibodies after the administration of factor IX concentrate (8). In patients with hemophilia B with antibodies, treatment with factor IX concentrate can result in an anaphylactic response. 

Erangie C, Lefaucheur C, Medioni J, Jacquot C, Flill GS, and Nochy D. 2007. Renal thrombotic microangiopathy caused by anti-VEGE-antibody treatment for metastatic renal-cell carcinoma. Lancet Oncol8 177-178. 

We also found that the mouse brain (as opposed to rat brain) does have ahigher degree of autofluorescence, which is the major limitation of doing fluorescence studies. However, we have found that dipping the processed tissue (after antibody treatment) in copper sulfate (1 h in 10 mM CuS04 in 50 mM NH4 acetate, pH 5.0) reduces the autofluorescence caused by lipofuscin. This technique does not work in other tissues, and the amount of autofluorescence can be quite high. 

---