Devoe Burford DEVOE BURFORD, LPC
Counselor/Therapist | Professional
510 HIGHWAY 51 S BATESVILLE MS, 38606About
Devoe Burford is a counselor in BATESVILLE, MS. Devoe evaluates patients using many different procedures, in order to determine what treatments must be carried out in order to properly assess their symptoms. Counselors provide consultation for each patient and their families.
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Transcriptional inhibition of stromelysin by interferon-gamma in normal human fibroblasts is mediated by the AP-1 domain.
- Relaxin deficiency in mice is associated with an age-related progression of pulmonary fibrosis.
- Relaxin regulates fibrillin 2, but not fibrillin 1, mRNA and protein expression by human dermal fibroblasts and murine fetal skin.
- Relaxin is a key mediator of prostate growth and male reproductive tract development.
- Vascular endothelial growth factor induces interstitial collagenase expression in human endothelial cells.
- Relaxin alone and in conjunction with interferon-gamma decreases collagen synthesis by cultured human scleroderma fibroblasts.
- Relaxin-1-deficient mice develop an age-related progression of renal fibrosis.
- The relaxin gene-knockout mouse: a model of progressive fibrosis.
- The relaxin gene knockout mouse: a model of progressive scleroderma.
- Constitutive expression of a 92-kD gelatinase (type V collagenase) by rheumatoid synovial fibroblasts and its induction in normal human fibroblasts by inflammatory cytokines.
- Stromelysin expression regulates collagenase activation in human fibroblasts. Dissociable control of two metalloproteinases by interferon-gamma.
- Connective tissue metabolism including cytokines in scleroderma.
- TGF-beta 1 accelerates wound healing: reversal of steroid-impaired healing in rats and rabbits.
- Bone morphogenetic protein-2b stimulation of growth and osteogenic phenotypes in rat osteoblast-like cells: comparison with TGF-beta 1.
- Rapid publication. TGF-beta 1 induces bone closure of skull defects.
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