Osteochondritis Dissecans in the Dog

Osteochondritis dissecans (OeD) is a manifestation of osteochondrosis characterized by a focal thickening of joint cartilage and subsequent dissection of a flap of this thickened cartilage away from the underlying subchondral bone. The etiology of this condition remains somewhat of a mystery; trauma, nutrition, ischemia, and hereditary abnormalities of ossification have all been suggested. The disease is usually seen in the faster growing members of large and giant breed dogs. The first clinical signs of lameness are usually noted when the dog is between 5 and 9 months of age. OCD is most commonly recognized in the proximal humerus, but is also found in the distal humerus, distal femur, and tibial tarsal bone. One case of OeD of the distal radius has been reported. Other manifestations of osteochondrosis include ununited anconeal process, fragmented coronoid process, and retained cartilage of metaphyseal growth plates. Current research suggests there may be some relationship between osteochondrosis and the development of cervical spondylolisthesis, slipped femoral capital epiphysis, and hip dysplasia

Root Canal Therapy for Fracture-Induced Endodontic Disease in the Dog

Endodontics is a division of veterinary dentistry that deals with pathologic conditions of the tooth pulp. Endodontic disease occurs whenever viable pump tissue is exposed and becomes infected. It is a common sequela to tooth fractures, and occurs less frequently following dental decay and severe periodontal disease. It is the second most common disease in the oral cavity of companion animals

Commonwealth of the Northern Mariana Islands Emergency Management and Homeland Security Statutory Authorities Summarized

This report is one of a series that profiles the emergency management and homeland security statutory authorities of the 50 states, the District of Columbia, the Commonwealth of the Northern Mariana Islands, the Commonwealth of Puerto Rico, and three territories (American Samoa, Guam, and the U.S. Virgin Islands). Each profile identifies the more significant elements of state statutes, generally as codified. This report focuses on the Northern Mariana Islands

Guam Emergency Management and Homeland Security Statutory Authorities Summarized

This report is one of a series that profiles the emergency management and homeland security statutory authorities of the 50 states, the District of Columbia, the Commonwealth of the Northern Mariana Islands, the Commonwealth of Puerto Rico, and three territories (American Samoa, Guam, and the U.S. Virgin Islands). Each profile identifies the more significant elements of state statutes, generally as codified. This report focuses on Guam

Propagation of blood clotting in the complex biochemical network of hemostasis is described by a simple mechanism

Hemostasis is the complex biochemical network that controls blood clotting. We previously described a chemical model that mimicked the dynamics of hemostasis based on a simple regulatory mechanisma threshold response due to the competition between production and removal of activators. Here, we used human blood plasma in phospholipid-coated microfluidic channels to test predictions based on this mechanism. We demonstrated that, for a given geometry of channels, clot propagation from an obstructed channel into a channel with flowing blood plasma is dependent on the shear rate in the channel with flowing blood plasma. If confirmed in vivo, these results may explain clot propagation from a small vessel to a larger, clinically relevant vessel. In addition, these results would further validate the use of modular mechanisms, simplified chemical models, and microfluidics to study complex biochemical networks

Effects of shear rate on propagation of blood clotting determined using microfluidics and numerical simulations

This paper describes microfluidic experiments with human blood plasma and numerical simulations to determine the role of fluid flow in the regulation of propagation of blood clotting. We demonstrate that propagation of clotting can be regulated by different mechanisms depending on the volume-to-surface ratio of a channel. In small channels, propagation of clotting can be prevented by surface-bound inhibitors of clotting present on vessel walls. In large channels, where surface-bound inhibitors are ineffective, propagation of clotting can be prevented by a shear rate above a threshold value, in agreement with predictions of a simple reaction-diffusion mechanism. We also demonstrate that propagation of clotting in a channel with a large volume-to-surface ratio and a shear rate below a threshold shear rate can be slowed by decreasing the production of thrombin, an activator of clotting. These in vitro results make two predictions, which should be experimentally tested in vivo. First, propagation of clotting from superficial veins to deep veins may be regulated by shear rate, which might explain the correlation between superficial thrombosis and the development of deep vein thrombosis (DVT). Second, nontoxic thrombin inhibitors with high binding affinities could be locally administered to prevent recurrent thrombosis after a clot has been removed. In addition, these results demonstrate the utility of simplified mechanisms and microfluidics for generating and testing predictions about the dynamics of complex biochemical networks