Publications by authors named "I M London"

Article Synopsis
  • Anti-drug antibodies linked to treatment failure in inflammatory bowel disease (IBD) patients on anti-TNF agents were analyzed in a large UK study involving 1058 participants.
  • The study found that patients who developed antibodies to their first anti-TNF drug were more likely to also develop antibodies to their second anti-TNF drug, indicating a potential pattern of immunogenicity across different treatments.
  • Introducing an immunomodulator when switching anti-TNF therapies boosted treatment persistence in patients with immunogenicity, suggesting that combined therapies may enhance outcomes in IBD management.
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Objectives: We describe the frequency and types of drug therapy problems (DTPs), and interventions carried out to resolve them, among a cohort of HIV-infected patients on ART in Jos, Nigeria.

Methods: A prospective pharmacists' intervention study was conducted between January and August 2012 at the outpatient HIV clinic of the Jos University Teaching Hospital (JUTH). Pharmacists identified DTPs and made recommendations to resolve them.

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A single nucleotide polymorphism (SNP) in the sickle beta-globin gene (beta(S)) leads to sickle cell anemia. Sickling increases sharply with deoxy sickle Hb concentration and decreases with increasing fetal gamma-globin concentration. Measures that decrease sickle Hb concentration should have an antisickling effect.

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Achieving long-term pancellular expression of a transferred gene at therapeutic level in a given hematopoietic lineage remains an important goal of gene therapy. Advances have recently been made in the genetic correction of the hemoglobinopathies by means of lentiviral vectors and large locus control region (LCR) derivatives. However, panerythroid beta globin gene expression has not yet been achieved in beta thalassemic mice because of incomplete transduction of the hematopoietic stem cell compartment and position effect variegation of proviruses integrated at a single copy per genome.

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Sickle cell disease (SCD) is caused by a single point mutation in the human betaA globin gene that results in the formation of an abnormal hemoglobin [HbS (alpha2betaS2)]. We designed a betaA globin gene variant that prevents HbS polymerization and introduced it into a lentiviral vector we optimized for transfer to hematopoietic stem cells and gene expression in the adult red blood cell lineage. Long-term expression (up to 10 months) was achieved, without preselection, in all transplanted mice with erythroid-specific accumulation of the antisickling protein in up to 52% of total hemoglobin and 99% of circulating red blood cells.

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