Publications by authors named "Richard Lundberg"

7 Publications

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Recommendations on bioanalytical method stability implications of co-administered and co-formulated drugs by Global CRO Council for Bioanalysis (GCC).

Bioanalysis 2012 Sep;4(17):2117-26

Advion Bioanalytical Laboratories, Quintiles, NY, USA.

An open letter written by the Global CRO Council for Bioanalysis (GCC) describing the GCC survey results on stability data from co-administered and co-formulated drugs was sent to multiple regulatory authorities on 14 December 2011. This letter and further discussions at different GCC meetings led to subsequent recommendations on this topic of widespread interest within the bioanalytical community over the past 2 years.
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http://dx.doi.org/10.4155/bio.12.192DOI Listing
September 2012

4th Global CRO Council for Bioanalysis: coadministered drugs stability, EMA/US FDA guidelines, 483s and carryover.

Bioanalysis 2012 Apr;4(7):763-8

The Global CRO Council for Bioanalysis (GCC) was formed in September 2010. Since then, the representatives of the member companies come together periodically to openly discuss bioanalysis and the regulatory challenges unique to the outsourcing industry. The 4th GCC Closed Forum brought together experts from bioanalytical CROs to share and discuss recent issues in regulated bioanalysis, such as the impact of coadministered drugs on stability, some differences between European Medicines Agency and US FDA bioanalytical guidance documents and lessons learned following recent Untitled Letters. Recent 483s and agency findings, as well as issues on method carryover, were also part of the topics discussed.
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http://dx.doi.org/10.4155/bio.12.48DOI Listing
April 2012

Analysis of total and transferrin-bound iron in human serum for pharmacokinetic studies of iron-sucrose formulations.

Bioanalysis 2011 Aug;3(16):1837-46

Research & Development Laboratory, MEDTOX Laboratories, New Brighton, MN 55112, USA.

Background: Patients with iron-deficiency anemia benefit from intravenous iron therapies. Development of these pharmaceutical agents requires pharmacokinetic studies monitoring levels of both the administered agent and transferrin-bound iron (TBI). Successful pharmacokinetic methods must discriminate iron species.

Results: Routine colorimetric procedures were used to reliably measure total iron and TBI following iron-sucrose administration. Iron was liberated from iron-sucrose allowing the determination of all circulating iron. Solid-phase sample processing allowed the measurement of TBI. Circulating iron-sucrose could then be calculated as the difference between total iron and TBI.

Conclusion: A reproducible and robust spectrophotometric method was developed and validated for measuring total iron and TBI in human serum following iron-sucrose therapy.
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http://dx.doi.org/10.4155/bio.11.180DOI Listing
August 2011

Intermediate DNA repair activity associated with the 322delG allele of the fanconi anemia complementation group C gene.

J Mol Biol 2004 Oct;342(5):1443-55

Department of Pharmacology, University of Minnesota Medical School, 6-120 Jackson Hall, 321 Church St. SE, Minneapolis, MN 55455, USA.

Fanconi anemia (FA) is an autosomal recessive disorder associated with pancytopenia and cancer susceptibility. The disorder is heterogeneous, with at least nine complementation groups having been identified. Several recent studies have suggested that defective plasmid DNA end-joining is a consistent feature of FA cells. It was therefore surprising to discover a strain of fibroblasts from an FA patient that possessed wild-type plasmid DNA end-joining activity. Unlike other FA strains, these fibroblasts have wild-type levels of homologous DNA recombination activity and are relatively insensitive to restriction endonuclease-induced death. Interestingly, while end-joining in a number of FA fibroblast strains belonging to complementation groups A, C, and D2 was approximately 70% precise, end-joining in this latter strain of fibroblasts was more than 95% imprecise. Analysis revealed that these latter cells harbored an allele of the FA C gene, referred to as 322delG, that encodes an amino-terminal truncated protein. The relative rarity of this allele precluded the analysis of other FA fibroblast strains; however, studies revealed that overexpression of this allele in normal cells recapitulated the DNA end-joining phenotype seen in the 322delG FA fibroblast strain. These results indicate that DNA end-joining in fibroblasts expressing the 322delG allele of the FA-C gene in fibroblasts is highly imprecise; however, the DNA repair efficiency of these cells is more normal than that commonly associated with FA fibroblasts. This conclusion is intriguing, since a number of reports have suggested that patients harboring this allele exhibit a milder clinical course than do individuals with other alleles of the FA-C gene.
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http://dx.doi.org/10.1016/j.jmb.2004.08.013DOI Listing
October 2004

Deficient regulation of DNA double-strand break repair in Fanconi anemia fibroblasts.

J Biol Chem 2003 Aug 14;278(32):29487-95. Epub 2003 May 14.

Department of Pharmacology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA.

Fibroblasts from patients with Fanconi anemia (FA) display genomic instability, hypersensitivity to DNA cross-linking agents, and deficient DNA end joining. Fibroblasts from two FA patients of unidentified complementation group also had significantly increased cellular homologous recombination (HR) activity. Results described herein show that HR activity levels in patient-derived FA fibroblasts of groups A, C, and G were 10-fold greater than those seen in normal fibroblasts. In contrast, HR activity in group D2 fibroblasts was identical to that in normal cells. Western blot analysis revealed that the RAD51 protein was elevated 10-fold above normal levels in group A, C, and G fibroblasts, but was not altered in group D2 fibroblasts. HR activity levels in these former cells could be restored to near-normal levels by electroporation with anti-RAD51 antibody, whereas similar treatment of normal and complementation group D2 fibroblasts had no effect. These findings are consistent with a model in which FA proteins function to coordinate DNA double-strand break repair activity by regulating both recombinational and non-recombinational DNA repair. Interestingly, whereas positive regulation of DNA end joining requires the combined presence of all FA proteins thus far tested, suppression of HR, which is minimally dependent on the FANCA, FANCC, and FANCG proteins, does not require FANCD2.
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http://dx.doi.org/10.1074/jbc.M213251200DOI Listing
August 2003