Brenda K Yoder RPT
Physical Therapist
901 N Curtis Rd Suite 204 Boise ID, 83706About
Brenda Yoder is a physical therapist practicing in Boise, ID. Brenda Yoder specializes in physical treatment to help a patient reduce pain, restore mobility, rehabilitate an injury, or increase movement and overall function. As a physical therapist, Brenda Yoder can treat multiple conditions with exercises, ultrasound, electrical stimulation, joint mobilization, heat, ice, massage, laser or light therapy and more. Brenda Yoder will create a treatment plan based on the patients specific injury or condition, and might target a specific body part or body system based on the individual.
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Expert Publications
Data provided by the National Library of Medicine- The Oak Ridge Polycystic Kidney (orpk) disease gene is required for left-right axis determination.
- Polaris, a protein involved in left-right axis patterning, localizes to basal bodies and cilia.
- The C. elegans homolog of the murine cystic kidney disease gene Tg737 functions in a ciliogenic pathway and is disrupted in osm-5 mutant worms.
- Gene expression and chromatin structure in the cellular slime mold, Dictyostelium discoideum.
- Articular cartilage and growth plate defects are associated with chondrocyte cytoskeletal abnormalities in Tg737orpk mice lacking the primary cilia protein polaris.
- Complement C3 activation in cyst fluid and urine from autosomal dominant polycystic kidney disease patients.
- Insertional mutagenesis and molecular analysis of a new gene associated with polycystic kidney disease.
- Oval cell proliferation associated with the murine insertional mutation TgN737Rpw.
- Isolation and characterization of liver epithelial cell lines from wild-type and mutant TgN737Rpw mice.
- The tetratricopeptide repeat containing Tg737 gene is a liver neoplasia tumor suppressor gene.
- The combination of epidermal growth factor and transforming growth factor-beta induces novel phenotypic changes in mouse liver stem cell lines.
- Characterization of growth factor responsiveness and alterations in growth factor homeostasis involved in the tumorigenic conversion of mouse oval cells.
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