Dr. Seth Jonathan Karp M.D.
Surgeon
110 Francis St The Transplant Cente Boston MA, 02215About
Dr. Seth Karp is a general surgeon practicing in Boston, MA. Dr. Karp specializes in abdominal contents including the esophagus, stomach, liver, gallbladder, pancreas and often thyroid glands. General surgeons are able to deal with almost any surgical or critical care emergency, also involving the skin or soft tissue trauma. Dr. Karp provides quality surgical service for gravely ill or injured patients and is able to respond quickly due to knowledge of various surgical procedures.
Board Certification
SurgeryAmerican Board of SurgeryABS
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Excellent outcomes after transplantation of deceased donor kidneys with high terminal creatinine and mild pathologic lesions.
- Restoration of liver mass after injury requires proliferative and not embryonic transcriptional patterns.
- Marginal donors in liver transplantation: expanding the donor pool.
- Optimized adeno-associated virus 8 produces hepatocyte-specific Cre-mediated recombination without toxicity or affecting liver regeneration.
- Donor postextubation hypotension and age correlate with outcome after donation after cardiac death transplantation.
- Roux limb volvulus after pancreas transplantation: an unusual cause of pancreatic graft loss.
- Tob1 is a constitutively expressed repressor of liver regeneration.
- A cross-sectional study of fatigue and sleep quality before and after kidney transplantation.
- Transcriptional ontogeny of the developing liver.
- New serum markers of hepatocellular carcinoma.
- BMP4 is a novel paracrine inhibitor of liver regeneration.
- Scar formation and lack of regeneration in adult and neonatal liver after stromal injury.
- Specific activin receptor-like kinase 3 inhibitors enhance liver regeneration.
- Biology of hepatocyte regeneration in acute liver failure.
- Cytometry-based single-cell analysis of intact epithelial signaling reveals MAPK activation divergent from TNF-α-induced apoptosis in vivo.
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