The Effect of the Histone Deacetylase Inhibitor Suberoylanilide Hydroxamic Acid and Paclitaxel Treatment on Full-Thickness Wound Healing in Mice.

Introduction: Neoadjuvant chemotherapy prior to lumpectomy or mastectomy for breast cancer challenges wound healing. Suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor, has been shown to work synergistically with paclitaxel in vitro and in preclinical studies. In addition, our laboratory has demonstrated that SAHA treatment decreases paclitaxel-associated stem cell toxicity, modulates inflammatory response, and promotes wound healing in injured fibroblast cells.

Acute kidney injury following implementation of an enhanced recovery after surgery (ERAS) protocol in colorectal surgery.

Purpose: Fluid management within Enhanced Recovery After Surgery (ERAS) protocols is designed to maintain a euvolemic state avoiding the negative sequelae of hypervolemia or hypovolemia. We sought to determine the effect of a recent ERAS protocol implementation on kidney function and on the incidence of postoperative acute kidney injury (AKI).

Methods: A total of 132 elective colorectal resections performed using our ERAS protocol were compared to a propensity-matched group prior to ERAS implementation.

Acceleration of diabetic wound healing with adipose-derived stem cells, endothelial-differentiated stem cells, and topical conditioned medium therapy in a swine model.

Objective: The purpose of our study was to investigate the effect of adipose-derived stem cells (ASCs), endothelial-differentiated ASCs (EC/ASCs), and various conditioned media (CM) on wound healing in a diabetic swine model. We hypothesized that ASC-based therapies would accelerate wound healing.

Methods: Diabetes was induced in four Yorkshire swine through intravenous injection of streptozotocin.

Antibodies to merkel cell polyomavirus T antigen oncoproteins reflect tumor burden in merkel cell carcinoma patients.

Merkel cell polyomavirus (MCPyV) is a common infectious agent that is likely involved in the etiology of most Merkel cell carcinomas (MCC). Serum antibodies recognizing the MCPyV capsid protein VP1 are detectable at high titer in nearly all MCC patients and remain stable over time. Although antibodies to the viral capsid indicate prior MCPyV infection, they provide limited clinical insight into MCC because they are also detected in more than half of the general population.