A complete carcinogen, Ultraviolet B radiation (290-320 nm; UVB), is the major cause of skin cancer. UVB-induced systemic immunosuppression that contributes to photocarcinogenesis is due to the glycerophosphocholine-derived lipid mediator Platelet-activating factor. A major question in photobiology is how UVB radiation, which only absorbs appreciably in the epidermal layers of skin, can generate systemic effects. UVB exposure and PAF Receptor (PAFR) activation in keratinocytes induce large amounts of microvesicle particle (extracellular vesicles 100-1000nm; MVP) release. MVPs released from skin keratinocytes in vitro in response to UVB (UVB-MVP) are dependent upon the keratinocyte PAFR. The present studies used both pharmacologic and genetic approaches in cells and mice to determine that both the PAFR and enzyme acid sphingomyelinase (aSMase) were necessary for UVB-MVP generation. Discovery that the calcium-sensing receptor is a keratinocyte-selective MVP marker allowed us to determine that UVB-MVP leaving the keratinocyte can be found systemically in mice and in human subjects following UVB. Moreover, UVB-MVP contain bioactive contents including PAFR agonists which allow them to serve as effectors for UVB downstream effects, in particular UVB-mediated systemic immunosuppression.
Urban trauma centres have recently noted a shift in the causative mechanism of facial fractures away from motor vehicle crashes (MVC) to blunt assaults (BA). This study was conducted to examine the incidence and aetiology of facial fractures at our institution as well as the relationship with alcohol and protective device use. Trauma registry records of all patients admitted to a level I trauma centre from 1 January 1988 to 1 January 1999 were reviewed. There were 13594 trauma admissions during the 11-year period. Facial fractures were sustained by 1429 patients (10.5%) and this group forms the subject of this study. MVC was the predominant aetiology (59.9%) followed by BA (18.8%). Facial fractures were found in 9.5% of restrained MVC patients compared to 15.4% of unrestrained patients (P<0.00l). Non-helmeted motorcyclists were four times more likely to sustain facial fractures (4.3% vs. 18.4%) than helmeted patients (P<0.00l). 39.6% of patients in the MVC group were legally intoxicated compared to 73.5% in the BA group (P<0.00l). 45.4% of unrestrained patients with facial fractures were intoxicated compared to 11.8% of restrained MVC patients with facial fractures (P<0.001). MVC continue to be the primary aetiology of facial fractures in our trauma population. Protective devices decrease the incidence of facial fractures. Lack of protective device use and the consumption of alcohol correlate with sustaining facial fractures.
Thermal burn injuries are an important environmental stressor that can result in considerable morbidity and mortality. The exact mechanism by which an environmental stimulus to skin results in local and systemic effects is an area of active research. One potential mechanism to allow skin keratinocytes to disperse bioactive substances is via microvesicle particles, which are subcellular bodies released directly from cellular membranes. Our previous studies have indicated that thermal burn injury of the skin keratinocyte in vitro results in the production of the lipid mediator platelet-activating factor (PAF). The present studies demonstrate that thermal burn injury to keratinocytes in vitro and human skin explants ex vivo, and mice in vivo generate microvesicle particles. Use of pharmacologic and genetic tools indicates that the optimal release of microvesicles is dependent upon the PAF receptor. Of note, burn injury-stimulated microvesicle particles do not carry appreciable protein cytokines yet contain high levels of PAF. These studies describe a novel mechanism involving microvesicle particles by which a metabolically labile bioactive lipid can travel from cells in response to environmental stimuli.
Helmets are effective in decreasing maxillofacial trauma in motorcycle crashes. The impact, however, of motorcycle crashes on the location and patterns of craniofacial injuries among helmeted versus unhelmeted patients has not been examined. In the present study, 331 injured motorcyclists were evaluated to compare the incidence of craniofacial and spinal injury in 77 (23%) helmeted and 254 (77%) nonhelmeted patients. Nonhelmeted motorcyclists were three times more likely to suffer facial fractures (5.2% vs. 16.1%) than those wearing helmets (p < 0.01). Skull fracture occurred in only one helmeted patient (1.2%), compared with 36 (12.3%) of nonhelmeted patients (p < or = 0.01). The incidence of spinal injury was not significantly different between the two groups. Blood alcohol levels demonstrated that 12% of the helmeted group were legally intoxicated (blood alcohol level > 100 mg/dL), in contrast to 37.9% of the nonhelmeted motorcyclists (p < or = 0.01). Failure to wear a helmet resulted in a significantly higher incidence of craniofacial injury among patients involved in motorcycle crashes, but did not affect spinal injury or mortality. Alcohol usage seemed to correlate with failure to use helmets. Helmet use should be legally mandated on a national level for all motorcyclists.
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