Use of a colorimeter is a viable method to measure melanin and erythema content in the context of laser beam attenuation by use of a class IV laser in different tissues in dogs.

Objective: Patient factors may alter laser photon attenuation, but these factors have not been adequately evaluated in live dogs. Our objective was to evaluate class IV laser beam attenuation (LBA) by canine tissues using a colorimeter to evaluate melanin and erythema indices. We hypothesized that greater melanin and erythema indices and unclipped hair would increase LBA, and these properties would vary among tissues.

Bilateral renal descensus and intravesicular ureteroneocystostomy for treatment of bilateral ureteral ligation and transection that occurred during ovariohysterectomy in two cats.

Case Description: 6-month-old and 7-month-old spayed female domestic shorthair cats were referred because of complications associated with inadvertent bilateral ureteral ligation and transection during ovariohysterectomy.

Clinical Findings: Both cats had a 1- to 2-day history of lethargy, inappetence, and vomiting. Initial exam findings included lethargy, signs of abdominal pain, anuria, and dehydration.

Non-immunogenic utrophin gene therapy for the treatment of muscular dystrophy animal models.

The essential product of the Duchenne muscular dystrophy (DMD) gene is dystrophin, a rod-like protein that protects striated myocytes from contraction-induced injury. Dystrophin-related protein (or utrophin) retains most of the structural and protein binding elements of dystrophin. Importantly, normal thymic expression in DMD patients should protect utrophin by central immunologic tolerance.

Suite of clinically relevant functional assays to address therapeutic efficacy and disease mechanism in the dystrophic mouse.

Duchenne muscular dystrophy (DMD) is a progressive primary myodegenerative disease caused by a genetic deficiency of the 427-kDa cytoskeletal protein dystrophin. Despite its single-gene etiology, DMD's complex pathogenesis remains poorly understood, complicating the extrapolation from results of preclinical studies in genetic homologs to the design of informative clinical trials. Here we describe novel phenotypic assays which when applied to the mouse resemble recently used primary end points for DMD clinical trials.