Surgical Treatment of Recurrent Rectal Prolapse in an Adult Female Black-crested Mangabey () by Colopexy.

A 13-y-old, multiparous female black-crested mangabey (Lophocebus aterrimus) underwent surgical treatment for chronically recurring rectal prolapse by laparotomy and subsequent colopexy. Initially, a laparoscopic approach was attempted but was converted to an open approach after intraabdominal adhesions were noted. The colopexy was performed through a ventral midline incision, with no complications intraoperatively or postoperatively.

Correction of biapical radial deformities by use of bi-level hinged circular external fixation and distraction osteogenesis in 13 dogs.

Objectives: To describe clinical, radiographic, and computed tomographic (CT) assessment of biapical deformities of the radius in dogs and evaluate the effectiveness of their management by use of bilevel hinged circular external fixation frames.

Study Design: Prospective, non-randomized cohort study.

Animals: Dogs (N = 26: 13 with 14 limbs operated, 13 controls).

Comparison of surgical site infection rates in clean and clean-contaminated wounds in dogs and cats after minimally invasive versus open surgery: 179 cases (2007-2008).

Objective: To report and compare the surgical site infection (SSI) rates for clean and clean-contaminated procedures performed by either a minimally invasive surgical or open surgical approach in a large population of dogs and cats.

Design: Prospective case series.

Animals: 179 patients (dogs and cats) undergoing minimally invasive abdominal or thoracic surgery.

The small heat shock protein HspB2 is a novel anti-apoptotic protein that inhibits apical caspase activation in the extrinsic apoptotic pathway.

Members of the conserved small heat shock protein (sHSP) family, such as αB-crystallin and Hsp27, are constitutively expressed in diverse malignancies and have been linked to several hallmark features of cancer including apoptosis resistance. In contrast, the sHSP HspB2/MKBP, which shares an intergenic promoter with αB-crystallin, was discovered as a chaperone of the myotonic dystrophy protein kinase and has not been previously implicated in apoptosis regulation. Here we describe a new function for HspB2 as a novel inhibitor of apical caspase activation in the extrinsic apoptotic pathway.

Aspirin sensitizes cancer cells to TRAIL-induced apoptosis by reducing survivin levels.

Purpose: Although tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and agonistic antibodies targeting its receptors are promising cancer therapies because of their tumor selectivity, many tumors are resistant to TRAIL-based therapies. We examined whether the nonsteroidal anti-inflammatory drug aspirin sensitized cancer cells to TRAIL agonists in vitro and in vivo and investigated the underlying mechanism.

Experimental Design: The effects of aspirin on sensitivity to TRAIL agonists and expression of apoptosis regulators was determined in human breast cancer cell lines and xenograft tumors.

The small heat shock protein alpha B-crystallin is a novel inhibitor of TRAIL-induced apoptosis that suppresses the activation of caspase-3.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor alpha family of cytokines that preferentially induces apoptosis in transformed cells, making it a promising cancer therapy. However, many neoplasms are resistant to TRAIL-induced apoptosis by mechanisms that are poorly understood. We demonstrate that the expression of the small heat shock protein alpha B-crystallin (but not other heat shock proteins or apoptosis-regulating proteins) correlates with TRAIL resistance in a panel of human cancer cell lines.

Peroxisome proliferator-activated receptor gamma agonists promote TRAIL-induced apoptosis by reducing survivin levels via cyclin D3 repression and cell cycle arrest.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising cancer therapy that preferentially induces apoptosis in cancer cells. However, many neoplasms are resistant to TRAIL by mechanisms that are poorly understood. Here we demonstrate that human breast cancer cells, but not normal mammary epithelial cells, are dramatically sensitized to TRAIL-induced apoptosis and caspase activation by peroxisome proliferator-activated receptor gamma (PPARgamma) agonists of the thiazolidinedione (TZD) class.