Dr. Christopher Higgins Lowrey M.D.
Hematologist (Blood Specialist) | Hematology
1 Medical Center Dr Dhmc, Department Of Lebanon NH, 03756About
Dr. Christopher Lowrey is a hematology internist practicing in Lebanon, NH. Dr. Lowrey specializes in cases of suspected blood disorders when a diagnosis is unclear and further medical care is needed. Hematology internists work with other specialists such as surgeons, radiation therapists and gynecologists in order to get a better understanding on the cases. Often, patients are asked to participate in clinical research that could result in more efficient treatment methods.
Board Certification
Internal MedicineAmerican Board of Internal MedicineABIM- Hematology
Internal MedicineAmerican Board of Internal MedicineABIM- 1988
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Targeted remodeling of human beta-globin promoter chromatin structure produces increased expression and decreased silencing.
- Long-term silencing of retroviral vectors is resistant to reversal by trichostatin A and 5-azacytidine.
- In vivo formation of a human beta-globin locus control region core element requires binding sites for multiple factors including GATA-1, NF-E2, erythroid Kruppel-like factor, and Sp1.
- An erythroid-specific chromatin opening element reorganizes beta-globin promoter chromatin structure and augments gene expression.
- Defensive applications of gene transfer technology in the face of bioterrorism: DNA-based vaccines and immune targeting.
- An Erythroid-Specific Chromatin Opening Element Increases beta-Globin Gene
- The effects of lead and cadmium on GATA-1 regulated erythroid gene expression.
- Expression of GATA-1 in a non-hematopoietic cell line induces beta-globin locus control region chromatin structure remodeling and an erythroid pattern of gene expression.
- Mechanism of DNase I hypersensitive site formation within the human globin locus control region.
- CpG hypomethylation in a large domain encompassing the embryonic beta-like globin genes in primitive erythrocytes.
- Developmental- and differentiation-specific patterns of human gamma- and beta-globin promoter DNA methylation.
- Neither DNA hypomethylation nor changes in the kinetics of erythroid differentiation explain 5-azacytidine's ability to induce human fetal hemoglobin.
- A cell stress signaling model of fetal hemoglobin induction: what doesn't kill red blood cells may make them stronger.
- Developmentally regulated extended domains of DNA hypomethylation encompass highly transcribed genes of the human beta-globin locus.
- Complex developmental patterns of histone modifications associated with the human beta-globin switch in primary cells.
Treatments
- Cancer, Sickle Cell Disease, Blood Cancers
Fellowships
- National Institutes of Health, Bethesda, MD, Hematology 1988
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