Prospective evaluation of the surgical stabilization and outcome of canine tibial plateau fractures in three cases.

OBJECTIVE: To report the surgical approaches and stabilization of lateral and medial tibial plateau fractures (TPF), as well as the long-term outcome following repair. STUDY DESIGN: Prospective series of three client-owned dogs. ANIMALS: Three dogs. METHODS: For the two lateral TPF cases (Unger type 41-B1), the surgical approach included separation of the lateral collateral ligament and long digital extensor tendon. The lateral meniscus was elevated to allow visualization of the tibial surface and assess fracture reduction. The first case was repaired using two 2.0 mm lag screws (with washers). The second case sustained a lateral TPF, fibular fracture and concurrent tubercle of Gerdy fracture. Both tibial fractures were stabilized using two 2.0 mm lag screws with washers and two 0.9 mm Kirschner wires (K-wires). A third case, diagnosed with an Unger type 41-B2 medial TPF, was treated using 0.9 mm K-wires and 22-gauge tension band. RESULTS: There were no major complications noted. One minor complication occurred (screw yield two weeks postoperatively). By 8 weeks, all patients reached clinical union with good limb function. Owners were contacted 9-36 months postoperatively. LOAD scores and examinations were performed for two of three patients; the third patient was not contactable after relocating out of state. Both cases with completed questionnaires had a LOAD score of 5/52. CONCLUSION: Tibial plateau fractures are rare in canine patients. While challenging, they can be successfully managed using a combination of lag screws, K-wires, and tension band. CLINICAL SIGNIFICANCE: Surgical stabilization of TPF is feasible and may reduce the risk of meniscal injury.

Stress-Induced Suppression of Food Intake in Overweight and Obese Adolescents.

OBJECTIVE: Overweight adolescents exhibit greater cortisol reactivity in response to acute stress and are more likely to eat in response to emotional cues, which suggest an increased susceptibility to stress-induced eating. The purpose of this study was to examine the biological (cortisol and α-amylase reactivity) and behavioral (caloric intake) responses to an acute stressor in overweight adolescents. METHODS: Fifty-one adolescents ages 14 to 19 years (47% female, 55% white; body mass index, 31.2 ± 0.8 kg/m) were exposed to the Trier Social Stress Test and a control condition on separate days. Immediately after each condition, participants were provided with snacks to eat at their leisure. Reactivity was assessed via salivary cortisol and α-amylase area under the curve (AUC), and adolescents were categorized as high or low reactors. RESULTS: Cortisol AUC was higher during the stress condition (19.6 ± 0.2 µg/dl · min) compared with the control condition (11.4 ± 0.9 µg/dl · min, p < .001). α-Amylase AUC was not different during the stress condition (9999 ± 987 U/ml · min) compared with the control condition (8762 ± 865 U/ml · min, p = .145). Overall, adolescents consumed fewer calories during the stress condition (488 ± 51 kcal) compared with the control condition (637 ± 42 kcal, p = .007). High cortisol reactors decreased their calorie consumption from the control condition (716 ± 52 kcal) to the stress condition (457 ± 53 kcal, p = .001), whereas low cortisol reactors did not change their consumption (stress: 518 ± 87 kcal versus control: 561 ± 62 kcal, p = .574). CONCLUSION: High cortisol reactivity in overweight adolescents resulted in decreased calorie consumption after an acute stressor. Further research is needed to understand the mechanisms underlying stress-induced suppression of food intake in overweight adolescents.

Community Violence Exposure and Stress Reactivity in African American and Non-Latino White Adolescents With Overweight/Obesity.

Adolescents who experience community violence are exposed to toxic stressors at a critical period of growth and development. The purpose of this study was to examine the relationship between community violence exposure and stress reactivity in African American and non-Latino white adolescents with overweight/obesity. Fifty-one adolescents (47% female, 55% African American; aged 14-19) participated in this study. Community violence was assessed using the Survey of Children's Exposure to Community Violence. Stress reactivity was assessed via salivary cortisol and alpha-amylase area under the curve (AUC) during a Trier Social Stress Test (TSST). Race was a significant predictor of alpha-amylase reactivity (ß = 10740±3665, p = 0.0006), with a higher alpha-amylase AUC observed in African American compared to non-Latino white adolescents. There was also a significant difference in the relationship between community violence exposure and alpha-amylase AUC by race (ß = -3561±1226, p = 0.007). At similar increases in violence exposure, African Americans demonstrated a significant decline in alpha-amylase AUC while non-Latino whites demonstrated a significant increase in alpha-amylase AUC. Neither race nor violence exposure were significant predictors of cortisol AUC and there were no significant differences in the relationship between community violence exposure and cortisol AUC by race (all p's > .05). These preliminary findings suggest exposure to community violence may act to exacerbate autonomic dysregulation in African American adolescents with overweight/obesity. Longitudinal studies are needed to confirm the mechanisms by which community violence exposure differentially impacts stress responses by race.

Vascular inflammation in obesity and sleep apnea.

BACKGROUND: Unrecognized obstructive sleep apnea (OSA) is highly prevalent in obesity. Both obesity and OSA are associated with vascular endothelial inflammation and increased risk for cardiovascular diseases. We investigated directly whether the endothelial alterations that are attributed commonly to obesity are in fact related to OSA. METHODS AND RESULTS: Seventy-one subjects with a body mass index ranging from normal to obese underwent attended polysomnography. To assess vascular inflammation and oxidative stress directly, we quantified the expression of nuclear factor-kappaB and nitrotyrosine by immunofluorescence in freshly harvested venous endothelial cells. To evaluate basal endothelial nitric oxide (NO) production and activity, we quantified the expression of endothelial NO synthase (eNOS) and phosphorylated eNOS. Vascular reactivity was measured by brachial artery flow-mediated dilation. Expression of eNOS and phosphorylated eNOS and flow-mediated dilation were significantly lower, whereas expression of nitrotyrosine was significantly greater in OSA patients (n=38) than in OSA-free subjects (n=33) regardless of central adiposity. Expression of nuclear factor-kappaB was greater in obese OSA patients than in obese OSA-free subjects (P=0.004). Protein expression and flow-mediated dilation were not significantly affected by increasing body mass index or central obesity in OSA patients and in OSA-free subjects. After 4 weeks of continuous positive airway pressure therapy, flow-mediated dilation and expression of eNOS and phosphorylated eNOS significantly increased whereas expression of nitrotyrosine and nuclear factor-kappaB significantly decreased in OSA patients who adhered to continuous positive airway pressure >/=4 hours daily. CONCLUSIONS: Untreated OSA rather than obesity is a major determinant of vascular endothelial dysfunction, inflammation, and elevated oxidative stress in obese patients.

Stress coping strategies and stress reactivity in adolescents with overweight/obesity.

This study explored the associations between the frequency and effectiveness of habitual stress coping strategies on physiological and psychological stress responses to an acute laboratory stressor in adolescents with overweight/obesity (51 adolescents; 47% female; ages 14-19 years). Coping strategies were assessed using the Schoolager's Coping Strategies Inventory. Acute physiological stress responses were measured as salivary cortisol and α-amylase output during the Trier Social Stress Test and during a control condition. Acute psychological stress was measured using a Likert-type scale, and systolic blood pressure (SBP) and heart rate were measured at baseline. Results revealed that higher coping effectiveness was associated with lower log-based α-amylase during the stress (ß = -0.025, p = 0.018) and control (ß = -0.030, p = 0.005) conditions, but not with cortisol across either condition (all ps > 0.05). SBP moderated the association between coping effectiveness and α-amylase during the stress condition, with higher coping effectiveness associated with lower α-amylase only among individuals with lower SBP (ß = 0.002, p = 0.027). Coping frequency was not associated with cortisol responses, neither was habitual stress coping strategies associated with psychological stress (all ps > 0.05). These findings provide preliminary evidence that effective use of stress coping strategies may provide a dampening effect on sympathetic activity in an at-risk adolescent population.

Increased internalization of complement inhibitor CD59 may contribute to endothelial inflammation in obstructive sleep apnea.

Obstructive sleep apnea (OSA), characterized by intermittent hypoxia (IH) during transient cessation of breathing, triples the risk for cardiovascular diseases. We used a phage display peptide library as an unbiased approach to investigate whether IH, which is specific to OSA, activates endothelial cells (ECs) in a distinctive manner. The target of a differentially bound peptide on ECs collected from OSA patients was identified as CD59, a major complement inhibitor that protects ECs from the membrane attack complex (MAC). A decreased proportion of CD59 is located on the EC surface in OSA patients compared with controls, suggesting reduced protection against complement attack. In vitro, IH promoted endothelial inflammation predominantly via augmented internalization of CD59 and consequent MAC deposition. Increased internalization of endothelial CD59 in IH appeared to be cholesterol-dependent and was reversed by statins in a CD59-dependent manner. These studies suggest that reduced complement inhibition may mediate endothelial inflammation and increase vascular risk in OSA patients.

Secondhand Smoking Is Associated With Vascular Inflammation.

BACKGROUND: The relative risk for cardiovascular diseases in passive smokers is similar to that of active smokers despite almost a 100-fold lower dose of inhaled cigarette smoke. However, the mechanisms underlying the surprising susceptibility of the vascular tissue to the toxins in secondhand smoke (SHS) have not been directly investigated. The aim of this study was to investigate directly vascular endothelial cell function in passive smokers. METHODS: Using a minimally invasive method of endothelial biopsy, we investigated directly the vascular endothelium in 23 healthy passive smokers, 25 healthy active smokers, and 23 healthy control subjects who had never smoked and had no regular exposure to SHS. Endothelial nitric oxide synthase (eNOS) function (expression of basal eNOS and activated eNOS [phosphorylated eNOS at serine1177 (P-eNOS)]) and expression of markers of inflammation (nuclear factor-κB [NF-κB]) and oxidative stress (nitrotyrosine) were assessed in freshly harvested venous endothelial cells by quantitative immunofluorescence. RESULTS: Expression of eNOS and P-eNOS was similarly reduced and expression of NF-κB was similarly increased in passive and active smokers compared with control subjects. Expression of nitrotyrosine was greater in active smokers than control subjects and similar in passive and active smokers. Brachial artery flow-mediated dilation was similarly reduced in passive and active smokers compared with control subjects, consistent with reduced endothelial NO bioavailability. CONCLUSIONS: Secondhand smoking increases vascular endothelial inflammation and reduces active eNOS to a similar extent as active cigarette smoking, indicating direct toxic effects of SHS on the vasculature.

Endothelial repair capacity and apoptosis are inversely related in obstructive sleep apnea.

PURPOSE: To investigate the impact of obstructive sleep apnea (OSA) on endothelial repair capacity and apoptosis in the absence of potentially confounding factors including obesity. PATIENTS AND METHODS: Sixteen patients with a body mass index <30 and newly diagnosed OSA and 16 controls were studied. Circulating levels of endothelial progenitor cells, a marker of endothelial repair capacity, and endothelial microparticles, a marker of endothelial apoptosis, were quantified before and after four-week therapy with continuous positive airway pressure (CPAP). Endothelial cell apoptotic rate was also quantified in freshly harvested venous endothelial cells. Vascular reactivity was measured by flow-mediated dilation. RESULTS: Before treatment, endothelial microparticle levels were greater and endothelial progenitor cell levels were lower in patients with OSA than in controls (P < 0.001 for both). Levels of endothelial microparticles and progenitors cells were inversely related (r = -0.67, P < 0.001). Endothelial progenitor cell levels increased after effective treatment (P = 0.036). CONCLUSIONS: In the absence of any co-morbid conditions including obesity, OSA alone impairs endothelial repair capacity and promotes endothelial apoptosis. These early endothelial alterations may underlie accelerated atherosclerosis and increased cardiovascular risk in OSA.