Search

Your search keyword '"Buko, Alex"' showing total 28 results
Start Over Author "Buko, Alex"
28 results on '"Buko, Alex"'

4. Distinctive Molecular and Metabolic Profiles of Chemically Synthesized Psilocybin and Psychedelic Mushroom Extract

Author

Lerer, Bernard, primary, Shahar, Orr, additional, Botvinnik, Alexander, additional, Shwartz, Amit, additional, Lerer, Elad, additional, Buko, Alex, additional, Hamid, Ethan, additional, Kahn, Dani, additional, Guralnick, Miles, additional, Blakolmer, Karin, additional, Wolf, Gilly, additional, Lerer, Leonard, additional, and Lifschytz, Tzuri, additional

Published
2023
Full Text
View/download PDF

6. Quality assessment and analysis of Biogen Idec compound library

Author

Bowes, Scott, Sun, Dongyu, Kaffashan, Azita, Zeng, Chenhui, Chuaqui, Claudio, Hronowski, Xiaoping, Buko, Alex, Zhang, Xin, and Josiah, Serene

Subjects
Mass spectrometry -- Usage -- Methods, Liquid chromatography -- Usage -- Methods, Drugs -- Product/Service Evaluations, Biological sciences, Usage, Methods
Abstract

A subset of the compound repository for lead identification at Biogen Idec was characterized for its chemical stability over a 3-year period. Compounds were stored at 4 °C as 10 [...]

Published
2006

9. Finding useful biomarkers for Parkinson’s disease

Author

Chen-Plotkin, Alice S., primary, Albin, Roger, additional, Alcalay, Roy, additional, Babcock, Debra, additional, Bajaj, Vikram, additional, Bowman, Dubois, additional, Buko, Alex, additional, Cedarbaum, Jesse, additional, Chelsky, Daniel, additional, Cookson, Mark R., additional, Dawson, Ted M., additional, Dewey, Richard, additional, Foroud, Tatiana, additional, Frasier, Mark, additional, German, Dwight, additional, Gwinn, Katrina, additional, Huang, Xuemei, additional, Kopil, Catherine, additional, Kremer, Thomas, additional, Lasch, Shirley, additional, Marek, Ken, additional, Marto, Jarrod A., additional, Merchant, Kalpana, additional, Mollenhauer, Brit, additional, Naito, Anna, additional, Potashkin, Judith, additional, Reimer, Alyssa, additional, Rosenthal, Liana S., additional, Saunders-Pullman, Rachel, additional, Scherzer, Clemens R., additional, Sherer, Todd, additional, Singleton, Andrew, additional, Sutherland, Margaret, additional, Thiele, Ines, additional, van der Brug, Marcel, additional, Van Keuren-Jensen, Kendall, additional, Vaillancourt, David, additional, Walt, David, additional, West, Andrew, additional, and Zhang, Jing, additional

Published
2018
Full Text
View/download PDF

10. JC Polyomavirus Abundance and Distribution in Progressive Multifocal Leukoencephalopathy (PML) Brain Tissue Implicates Myelin Sheath in Intracerebral Dissemination of Infection

Author

Wharton, Keith A., primary, Quigley, Catherine, additional, Themeles, Marian, additional, Dunstan, Robert W., additional, Doyle, Kathryn, additional, Cahir-McFarland, Ellen, additional, Wei, Jing, additional, Buko, Alex, additional, Reid, Carl E., additional, Sun, Chao, additional, Carmillo, Paul, additional, Sur, Gargi, additional, Carulli, John P., additional, Mansfield, Keith G., additional, Westmoreland, Susan V., additional, Staugaitis, Susan M., additional, Fox, Robert J., additional, Meier, Werner, additional, and Goelz, Susan E., additional

Published
2016
Full Text
View/download PDF

11. JC Polyomavirus Abundance and Distribution in Progressive Multifocal Leukoencephalopathy (PML) Brain Tissue Implicates Myelin Sheath in Intracerebral Dissemination of Infection.

Author

Jr.Wharton, Keith A., Quigley, Catherine, Themeles, Marian, Dunstan, Robert W., Doyle, Kathryn, Cahir-McFarland, Ellen, Wei, Jing, Buko, Alex, Reid, Carl E., Sun, Chao, Carmillo, Paul, Sur, Gargi, Carulli, John P., Mansfield, Keith G., Westmoreland, Susan V., Staugaitis, Susan M., Fox, Robert J., Meier, Werner, and Goelz, Susan E.

Subjects
PROGRESSIVE multifocal leukoencephalopathy, POLYOMAVIRUS diseases, BRAIN physiology, RARE diseases, IMMUNOCOMPROMISED patients, IMMUNOMODULATORS, MEDICATION safety
Abstract

Over half of adults are seropositive for JC polyomavirus (JCV), but rare individuals develop progressive multifocal leukoencephalopathy (PML), a demyelinating JCV infection of the central nervous system. Previously, PML was primarily seen in immunosuppressed patients with AIDS or certain cancers, but it has recently emerged as a drug safety issue through its association with diverse immunomodulatory therapies. To better understand the relationship between the JCV life cycle and PML pathology, we studied autopsy brain tissue from a 70-year-old psoriasis patient on the integrin alpha-L inhibitor efalizumab following a ~2 month clinical course of PML. Sequence analysis of lesional brain tissue identified PML-associated viral mutations in regulatory (non-coding control region) DNA, capsid protein VP1, and the regulatory agnoprotein, as well as 9 novel mutations in capsid protein VP2, indicating rampant viral evolution. Nine samples, including three gross PML lesions and normal-appearing adjacent tissues, were characterized by histopathology and subject to quantitative genomic, proteomic, and molecular localization analyses. We observed a striking correlation between the spatial extent of demyelination, axonal destruction, and dispersion of JCV along white matter myelin sheath. Our observations in this case, as well as in a case of PML-like disease in an immunocompromised rhesus macaque, suggest that long-range spread of polyomavirus and axonal destruction in PML might involve extracellular association between virus and the white matter myelin sheath. [ABSTRACT FROM AUTHOR]

Published
2016
Full Text
View/download PDF

15. Implication of P450-Metabolite Complex Formation in the Nonlinear Pharmacokinetics and Metabolic Fate of (±)-(1′R*,3R*)-3-Phenyl-1-[(1′,2′,3′,4′-tetrahydro-5′,6′-methylene-dioxy-1′-naphthalenyl) methyl] pyrrolidine methanesulfonate (ABT-200) in Dogs

Author

Ferrero, James L., primary, Thomas, Samuel B., additional, Marsh, Kennan C., additional, Rodrigues, A. David, additional, Uchic, John T., additional, and Buko, Alex M., additional

Published
2002
Full Text
View/download PDF

16. Inhibition of p56lckTyrosine Kinase by Isothiazolones

Author

Trevillyan, James M, primary, Chiou, X.Grace, additional, Ballaron, Stephen J, additional, Tang, Qing M, additional, Buko, Alex, additional, Sheets, Michael P, additional, Smith, Morey L, additional, Putman, C.Brent, additional, Wiedeman, Paul, additional, Tu, Noah, additional, Madar, David, additional, Smith, Harriet T, additional, Gubbins, Earl J, additional, Warrior, Usha P, additional, Chen, Yung-Wu, additional, Mollison, Karl W, additional, Faltynek, Connie R, additional, and Djurić, Stevan W, additional

Published
1999
Full Text
View/download PDF

22. Fragmentation of a highly purified monoclonal antibody attributed to residual CHO cell protease activity.

Author

Gao, Sharon X., Ying Zhang, Stansberry-Perkins, Kensey, Buko, Alex, Shujun Bai, Nguyen, Vanessa, and Brader, Mark L.

Subjects
MONOCLONAL antibodies, FRAGMENTATION reactions, PROTEOLYTIC enzymes, ENZYMES, BIOTECHNOLOGY
Abstract

The article discusses a study on monoclonal antibody (mAb) fragmentation which is a degradation route that affects the quality of liquid drug products. It states that a better understanding of the degradation process is needed in order to control its deleterious effects on biotechnical products. A high-purity human IgG1 mAb which exhibited fragmentation was examined. The fragmentation was attributed to proteolytic enzyme activity which was detected by the use of a proteolytic enzyme inhibitor pepstatin A.

Published
2011
Full Text
View/download PDF

25. Implication of P450-metabolite complex formation in the nonlinear pharmacokinetics and metabolic fate of (+/-)-(1'R*,3R*)-3-phenyl-1-[(1',2',3',4'-tetrahydro-5',6'-methylene-dioxy-1'-naphthalenyl) methyl] pyrrolidine methanesulfonate (ABT-200) in dogs.

Author

L, Ferrero James, B, Thomas Samuel, C, Marsh Kennan, David, Rodrigues A, T, Uchic John, and M, Buko Alex

Abstract

Following a single oral or intravenous administration of the R,R(+) and S,S(-) (14)C-pseudoracemate of (+/-)-(1'R*,3R*)-3-phenyl-1-[(1',2',3',4'-tetrahydro-5',6'-methylene-dioxy-1'-naphthalenyl) methyl] pyrrolidine methanesulfonate (ABT-200/I) to dogs, a total of six (R,R[+]) and eight (S,S[-]) metabolites were identified by high-pressure liquid chromatography/mass spectral techniques. Greater than 99% of the dose was eliminated as metabolites indicating that the clearance of I was predominantly metabolic. The catechol was the major excreted metabolite (fecal), whereas the urine and bile predominantly contained metabolites resulting from secondary biotransformation of the catechol via O-methylation, glucuronidation, and sulfation. After a single 12 mg/kg oral dose of racemic I to dogs, the mean area under the plasma curve (AUC(0-24h)) averaged 4.55 micro g. h/ml, with an apparent plasma clearance value of 2.70 l/h. kg. After 14 daily doses, the apparent plasma clearance was 3.5-fold lower (0.78 l/h. kg) and the AUC(0-24h) about 4-fold higher (18.58 micro g. h/ml). Isolation of liver microsomes from these animals indicated that a cytochrome p450 (p450)-metabolite complex (MI complex) was formed in the liver after both single and multiple dosing. The mean concentration of the MI complex 24 h after a single dose averaged 31 pmol/mg of microsomal protein, whereas the amount in the animals given multiple doses of I averaged 163 pmol/mg. There was a positive correlation (R(2) = 0.993) between the plasma AUC for I and the amount of the MI complex found in the liver of each animal. Formation of the MI complex was demonstrated in vitro in control dog liver microsomes, was NADPH-dependent, and was dissociated from p450 with 2-methylbenzimidazole. In vitro preincubation studies indicated that I was a mechanism-based inhibitor and that formation of the complex inhibited catechol formation. These results demonstrate that the liver p450s that metabolize I form an inhibitory MI complex after in vivo administration in dogs. Formation of the complex increases during multiple dosing and inhibits the enzymes from further metabolism of I resulting in nonlinear pharmacokinetics.

Published
2002

28. Implication of P450-metabolite complex formation in the nonlinear pharmacokinetics and metabolic fate of (+/-)-(1'R*,3R*)-3-phenyl-1-[(1',2',3',4'-tetrahydro-5',6'-methylene-dioxy-1'-naphthalenyl) methyl] pyrrolidine methanesulfonate (ABT-200) in dogs.

Author

Ferrero JL, Thomas SB, Marsh KC, Rodrigues AD, Uchic JT, and Buko AM

Subjects
Animals, Bile enzymology, Cytochrome P-450 Enzyme System urine, Dogs, Feces enzymology, Male, Microsomes, Liver drug effects, Microsomes, Liver enzymology, Nonlinear Dynamics, Pyrrolidines administration & dosage, Pyrrolidines chemistry, Cytochrome P-450 Enzyme System metabolism, Pyrrolidines pharmacokinetics
Abstract

Following a single oral or intravenous administration of the R,R(+) and S,S(-) (14)C-pseudoracemate of (+/-)-(1'R*,3R*)-3-phenyl-1-[(1',2',3',4'-tetrahydro-5',6'-methylene-dioxy-1'-naphthalenyl) methyl] pyrrolidine methanesulfonate (ABT-200/I) to dogs, a total of six (R,R[+]) and eight (S,S[-]) metabolites were identified by high-pressure liquid chromatography/mass spectral techniques. Greater than 99% of the dose was eliminated as metabolites indicating that the clearance of I was predominantly metabolic. The catechol was the major excreted metabolite (fecal), whereas the urine and bile predominantly contained metabolites resulting from secondary biotransformation of the catechol via O-methylation, glucuronidation, and sulfation. After a single 12 mg/kg oral dose of racemic I to dogs, the mean area under the plasma curve (AUC(0-24h)) averaged 4.55 micro g. h/ml, with an apparent plasma clearance value of 2.70 l/h. kg. After 14 daily doses, the apparent plasma clearance was 3.5-fold lower (0.78 l/h. kg) and the AUC(0-24h) about 4-fold higher (18.58 micro g. h/ml). Isolation of liver microsomes from these animals indicated that a cytochrome p450 (p450)-metabolite complex (MI complex) was formed in the liver after both single and multiple dosing. The mean concentration of the MI complex 24 h after a single dose averaged 31 pmol/mg of microsomal protein, whereas the amount in the animals given multiple doses of I averaged 163 pmol/mg. There was a positive correlation (R(2) = 0.993) between the plasma AUC for I and the amount of the MI complex found in the liver of each animal. Formation of the MI complex was demonstrated in vitro in control dog liver microsomes, was NADPH-dependent, and was dissociated from p450 with 2-methylbenzimidazole. In vitro preincubation studies indicated that I was a mechanism-based inhibitor and that formation of the complex inhibited catechol formation. These results demonstrate that the liver p450s that metabolize I form an inhibitory MI complex after in vivo administration in dogs. Formation of the complex increases during multiple dosing and inhibits the enzymes from further metabolism of I resulting in nonlinear pharmacokinetics.

Published
2002
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results