Publications

BACKGROUND

Skateboarding is a popular recreational activity but has attendant associated risks. To place this risk in perspective, participation-based rates of injury were determined and compared with those of other selected sports. Skateboard-associated injuries were evaluated over time to determine participation-based trends in injury prevalence.

METHODS

Rates of skateboard-associated injury were studied for the 12-year period 1987 to 1998 for participants aged 7 years or older. The National Electronic Injury Surveillance System provided injury estimates for skateboarding and the selected additional sporting activities. The National Sporting Goods Association annual survey of nationally representative households provided participation estimates. A participation-based rate of injury was calculated from these data sets for the selected sports for the year 1998.

RESULTS

The 1998 rate of emergency department-treated skateboard-associated injuries-8.9 injuries per 1,000 participants (95% confidence interval [CI], 6.2, 11.6)-was twice as high as in-line skating (3.9 [95% CI, 3.1, 4.8]) and half as high as basketball (21.2 [95% CI, 18.3, 24.1]). The rate of skateboard-associated injuries declined from 1987 to 1993 but is again increasing: the 1998 rate was twice that of 1993 (4.5 [95% CI, 1.6, 7.4] and 8.9 [95% CI, 6.2, 11.6], respectively). Increases occurred primarily among adolescent and young adult skateboarders. The most frequent injuries in 1998 were ankle strain/sprain and wrist fracture: 1.2 (95% CI, 0.8, 1.6) and 0.6 (95% CI, 0.4, 0.8) per 1,000, respectively. Skateboard-associated injuries requiring hospitalization occurred in 2.9% and were 11.4 (95% CI, 7.5, 17.5) times more likely to have occurred as a result of a crash with a motor vehicle than injuries in those patients not hospitalized.

CONCLUSION

This study is the first to relate skateboarding and other sport injuries to participation exposures. We found that skateboarding is a comparatively safe sport; however, increased rates of injury are occurring in adolescent and young adult skateboarders. The most common injuries are musculoskeletal; the more serious injuries resulting in hospitalization typically involve a crash with a motor vehicle. This new methodology that uses participation-based injury rates might contribute to more effective injury control initiatives.

Bradykinin-induced mechanical hyperalgesia is sympathetically dependent and B(2)-type bradykinin receptor-mediated in the rat; however, a sympathetically independent component of bradykinin hyperalgesia is shown after subdiaphragmatic vagotomy. We evaluated the mechanism of this bradykinin-induced sympathetic-independent mechanical hyperalgesia. The dose-response curve for bradykinin mechanical hyperalgesia in sympathectomized plus vagotomized rats was similar in magnitude to that for sympathetically dependent bradykinin hyperalgesia in normal rats. Although bradykinin mechanical hyperalgesia was mediated by the B(2)-type bradykinin receptors after sympathectomy plus vagotomy, it had a much more rapid latency to onset. This hyperalgesia was significantly attenuated by inhibition of protein kinase A but not protein kinase C, similar to the hyperalgesia produced by prostaglandin E(2), an agent that directly sensitizes primary afferent nociceptors. However, unlike prostaglandin E(2)-induced mechanical hyperalgesia in normal rats, after sympathectomy plus vagotomy, bradykinin-induced hyperalgesia was not attenuated by inhibition of nitric oxide synthesis. Peripheral administration of a mu opioid agonist, [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin, significantly attenuated bradykinin mechanical hyperalgesia after sympathectomy plus vagotomy. These data suggest that after sympathectomy plus subdiaphragmatic vagotomy, bradykinin acts directly on primary afferents to produce mechanical hyperalgesia via a novel protein kinase A-dependent signaling mechanism.

Although an interspecific trade-off between competitive and colonizing ability can permit multispecies coexistence, whether this mechanism controls the structure of natural systems remains unresolved. We used models to evaluate the hypothesized importance of this trade-off for explaining coexistence and relative abundance patterns in annual plant assemblages. In a nonspatial model, empirically derived competition-colonization trade-offs related to seed mass were insufficient to generate coexistence. This was unchanged by spatial structure or interspecific variation in the fraction of seeds dispersing globally. These results differ from those of the more generalized competition-colonization models because the latter assume completely asymmetric competition, an assumption that appears unrealistic considering existing data for annual systems. When, for heuristic purposes, completely asymmetric competition was incorporated into our models, unlimited coexistence was possible. However, in the resulting abundance patterns, the best competitors/poorest colonizers were the most abundant, the opposite of that observed in natural systems. By contrast, these natural patterns were produced by competition-colonization models where environmental heterogeneity permitted species coexistence. Thus, despite the failure of the simple competition-colonization trade-off to explain coexistence in annual plant systems, this trade-off may be essential to explaining relative abundance patterns when other processes permit coexistence.

OBJECTIVES

This study focuses on the comorbidity between depression and diabetes, as well as depression and obesity, in a biracial community sample of older adults.

METHODS

The data are drawn from a cross-sectional survey of five counties in North Carolina, USA, part of a longitudinal study of morbidity and mortality among elders in the urban and rural south. During the first wave of the survey, 4162 persons 65+ years of age participated in an interview at their homes. During this interview, data were collected to assess demographics, functional status, cognitive status, depression and self-report of diabetes. In addition, subjects were asked to estimate their height and weight for the interviewers, from which data body mass index (BMI) was estimated.

RESULTS

In both uncontrolled and controlled analyses, female gender, lower education, functional impairment and cognitive impairment were associated with comorbid depression/diabetes and depression/high BMI. Age was not associated with comorbid depression/diabetes but younger age was associated with depression/cognitive impairment. African American race was strongly associated with depression/diabetes but not with depression/high BMI.

CONCLUSIONS

More studies of comorbidity in the general population should be implemented to determine the relationship between these comorbid conditions and risk factors. Longitudinal studies are especially needed.