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Richard F. Branda

Researcher at University of Vermont

Publications -  50
Citations -  2100

Richard F. Branda is an academic researcher from University of Vermont. The author has contributed to research in topics: Chinese hamster ovary cell & Peripheral blood mononuclear cell. The author has an hindex of 26, co-authored 50 publications receiving 2061 citations. Previous affiliations of Richard F. Branda include University of Southampton.

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Mechanism of factor VIIa-dependent coagulation in hemophilia blood.

TL;DR: Pharmacologic concentrations of factor VIIa cannot restore normal thrombin generation in hemophilia A and hemophili B blood in vitro, and the efficacy offactor VIIa (10-50 nM) in hemophile blood is dependent on TF.
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Blood Coagulation in Hemophilia A and Hemophilia C

TL;DR: Coagulation in hemophilia A blood at 25 pmol/L TF is impaired, with significantly slower thrombin generation than normal during the propagation phase; this reducedThrombin appears to affect FPA production and factor V activation more profoundly than platelet activation.
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Immune stimulation by an antisense oligomer complementary to the rev gene of HIV-1.

TL;DR: Observations are consistent with the possibility that DNA sequences homologous to the rev gene participate in the regulation of mammalian lymphocyte activation, proliferation and maturation.
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Amplification of antibody production by phosphorothioate oligodeoxynucleotides

TL;DR: Results indicate that the unmethylated anti-rev oligomer is the most potent of the phosphorothioate oligomers tested at activating lymphocyte proliferation and differentiation and that a single intravenous injection of this oligodeoxynucleotide augments antibody production to a specific antigen as long as 35 days later.
Journal Article

Folate deficiency increases genetic damage caused by alkylating agents and gamma-irradiation in Chinese hamster ovary cells.

TL;DR: Folate deficiency acts synergistically with alkylating agents to increase somatic mutation and with gamma-irradiation to promote DNA strand breaks in CHO cells, indicating that folate deficiency appears to potentiate the genetic damage caused by mutagens/carcinogens by limiting DNA repair.