Incisional wound healing in the canine oral mucosa was histologically monitored at 3, 7, and 14 days after incision. Healing was compared from a scalpel, a carbon dioxide (CO2) laser at 10.6 microm, and the Vanderbilt free-electron laser tuned to 6.0, 6.45, and 6.8 microm. A significant delay in wound healing was observed when incisions were made with the CO2 laser, probably attributable to the excess thermal damage caused by the continuous-wave laser beam. When using the short pulsed, free-electron laser, a much smaller delay comparable to the scalpel wound healing was observed. This smaller delay tended to decrease with increasing tissue absorption. The results emphasize the greater importance of laser pulse duration rather than wavelength in relation to the subsequent wound healing.

P neumocystis species are opportunistic fungal pathogens that cause severe pneumonia in immunocompromised hosts, including AIDS patients. Clearance of Pneumocystis organisms is dependent on effective CD4ϩ T and B cell and macrophage responses (1-4). Failure to clear Pneumocystis organisms leads to severe alveolar damage due to the exaggerated inflammatory immune response (5). In spite of a reduced incidence of Pneumocystis pneumonia (PcP) in HIV-infected individuals due to improved antiviral therapies, the mortality rate for patients with PcP has not improved with the implementation of highly active antiretroviral therapy (HAART) (6). Additional studies are required to inform novel approaches to reduce morbidity and mortality due to Pneumocystis pneumonia.Outbreaks of PcP were first described in malnourished or premature infants in orphanages following the Second World War (7). Evidence suggests that immunocompetent individuals of all ages are capable of mounting protective immune responses to Pneumocystis jirovecii that prevent progression to pneumonia. Most children encounter this opportunistic fungus at a young age, as indicated by the presence of specific antibodies in the sera of 85% of individuals by the age of 3 years (8). Previous work from our lab has shown that the neonatal mouse immune response to Pneumocystis is delayed, due in part to an anti-inflammatory lung environment (9-12). The neonatal lung environment is characterized by anti-inflammatory mediators, including transforming growth factor ␤1 (TGF-␤1) and interleukin 10 (IL-10), and immature immune cells (9-12). Neonatal alveolar macrophages and T cells adoptively transferred to an adult lung environment are competent at resolving Pneumocystis murina pneumonia in mice (9, 12). In addition, neonatal alveolar macrophages are deficient in NF-B translocation following stimulation with Pneumocystis organisms (9). Neonatal alveolar CD11c ϩ cells demonstrate delayed trafficking to the draining lymph nodes (11). Together, these data indicate that both the neonatal lung environment and intrinsic immune cell deficits contribute to the delayed clearance of P. murina in neonatal mice.Pneumocystis species have a biphasic life cycle. Trophic forms are proposed to represent the asexual stage of the life cycle, whereas cysts are the ascus-like sexual stage (13). Trophic forms are single-nucleated organisms that are typically found in clusters surrounded by a biofilm-like substance consisting of a conglomeration of DNA, ␤-glucan, and other sugars (14). Cysts are ascuslike structures that consist of multiple nuclei surrounded by a fungal cell wall. ␤-1,3-Glucan and ␤-1,6-glucan serve as the structural components of the cyst wall (15, 16). Trophic forms do not express ␤-glucan (15). Both stages express surface glycoproteins and mannoproteins, which may serve as pathogen-associated molecular patterns (PAMPs) that could interact with receptors on phagocytic cells (17)(18)(19). Neither life form expresses chitin or ␣-glucans (20).Dendritic cells are the principal ant...

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Posterior glottic stenosis is a disabling disease in which the vocal folds are fixed near the midline. This allows adequate vocal fold adduction for voicing, but does not permit useful abduction for ventilation. The most common cause is prolonged endotracheal intubation for mechanical ventilation, and the incidence is estimated at 4% for intubations between 5 and 10 days. Currently, our understanding and treatment modalities are based on retrospective reviews of small, nonrandomized clinical experiences. The purpose of this project was to develop an animal model that would improve our understanding of histologic changes and allow future prospective randomized trials for therapeutic intervention. Twelve dogs, 15 to 25 kg, were randomly divided into three groups. Animals in group I had a superficial injury produced in the tissue over the right cricoarytenoid joint; animals in group 2 had a deep soft tissue injury produced; and animals in group 3 underwent joint opening. The animals were allowed to recover for 2 months. Morphometric analysis of the harvested larynges demonstrated clinically significant limitation in motion in the animals with deep soft tissue injury and in animals with joint disruption. Histologic analysis revealed various degrees of injury, from loss of subepithelial soft tissue to cartilaginous resorption and fusion of the arytenoid to the cricoid. These findings were directly related to the depth of the initial injury. It is possible to produce posterior glottic stenosis in the canine species. This will serve as a reliable animal model for future study.

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