OBJECTIVES. This study focuses on the pattern of incidence, mechanisms, and circumstances of accident and injury in a series of pediatric patients who sustained dog bites.METHODS. In our retrospective survey, the medical charts of all children who were younger than 17 years and sought medical attention after a dog bite between 1994 and 2003 were reviewed. To obtain the total number of each dog breed in the administrative district, we analyzed 5873 files from the community dog registers. For establishment of a risk index, the representation of a dog breed among the total canine population was divided by the frequency of dog bites from this breed.RESULTS. A total of 341 children (mean age: 5.9 years) were identified. The annual incidence of dog bites was 0.5 per 1000 children between 0 and 16 years of age. Incidence was highest in 1-year-old patients and decreased with increasing age. The relative risk for a dog attack by a German shepherd or a Doberman was ϳ5 times higher than that of a Labrador/retriever or cross-breed. The vast majority (82%) of the dogs were familiar to the children. Most (322; 94%) of the children had injuries to 1 body region; in the remaining 19 (6%) children, up to 3 body regions were injured. Of 357 injuries, the face, head, and neck region was the leading site affected (50%). Inpatient treatment was required in 93 (27%) patients.CONCLUSIONS. Dog bites in children are frequent and influenced by the breed-related behavior of dogs, dog owners, children, and parents. Therefore, prevention strategies should focus on public education and training of dogs and their owners. Children who are younger than 10 years represent the high-risk group for dog attacks.www.pediatrics.org/cgi

Abstract-There is a growing body of evidence that inflammation might play an important role in the initiation and progression of cardiovascular diseases (CVDs). The designation of CVD as a chronic inflammatory process is further supported by evidence that the risk factors for CVD cause endothelial cells throughout the vascular tree to assume an inflammatory phenotype. These activated endothelial cells characteristically exhibit oxidative stress and increased adhesiveness for circulating leukocytes. Although initial efforts to define the mechanisms underlying the inflammatory phenotype in diseased endothelial cells have focused on the linkage between oxidative stress and adhesion molecule activation/expression, recent work has implicated a variety of additional factors that can modulate the magnitude and/or nature of the inflammatory responses in CVD. Platelets, angiotensin II, and the CD40/CD40 ligand signaling system are gaining recognition as contributors to the pathogenesis of CVD. These factors appear to converge with known pathways that link oxidative stress with adhesion molecule expression and help to explain the apparent integration of coagulation with inflammation in CVD. These factors also hold the promise of offering multiple sites for therapeutic intervention in CVD. Key Words: oxidative stress Ⅲ integrins Ⅲ angiotensin II Ⅲ adhesion molecules I nflammation is gaining widespread attention for its role in the initiation and progression of cardiovascular disease (CVD). Epidemiological studies have revealed strong associations between biochemical markers of systemic inflammation and both the presence of and future risk for symptomatic CVD. Animal experimentation as well as clinical studies has provided convincing evidence that the known risk factors for CVD (hypertension, diabetes, hypercholesterolemia, and smoking) can elicit both an inflammatory and a prothrombogenic phenotype in the vascular system. The phenotypic changes are more pronounced in endothelial cells and can include oxidative stress, increased expression of endothelial cell adhesion molecules (CAMs), activation of cell signaling pathways (eg, the CD40/CD40 ligand [CD40L] dyad), and the consequent adhesion and activation of leukocytes and platelets. In the microcirculation, the inflammatory manifestations of CVD are more readily visible in postcapillary venules. There is growing evidence, however, that the endothelium-dependent arteriolar dysfunction often associated with CVD is also linked to the systemic inflammatory response. [1][2][3][4] Because the expression of adhesion glycoproteins by activated endothelial cells is a rate-determining step in the recruitment of inflammatory cells, much attention has been devoted to the role of endothelial CAMs in CVD. This attention has produced considerable evidence for the: (1) altered endothelial CAM expression in animal models of CVD 2,5 ; (2) use of circulating levels of soluble endothelial CAMs (eg, soluble intercellular adhesion molecule-1 [sICAM-1]) as a marker for the severity of inflammati...

No abstract

Abstract-Hypercholesterolemia elicits an inflammatory response in the microvasculature that is accompanied by an increased expression of angiotensin II type-1 receptors (AT1-R) on platelets, leukocytes, and endothelial cells. AT1-R blockade attenuates inflammatory responses to angiotensin II (eg, adhesion molecule expression and reactive oxygen species production). We investigated whether AT1-R antagonism attenuates the platelet and leukocyte recruitment induced by acute hypercholesterolemia in postcapillary venules. Leukocyte and platelet adhesion and oxidative stress were quantified by intravital microscopy in cremaster muscle, and P-selectin and AT1-R expression was determined in mice placed on a normal diet (ND) or high-cholesterol diet (HCD) for 2 weeks. Platelet and leukocyte adhesion was significantly elevated by hypercholesterolemia. In HCD mice receiving losartan (HCD-Los) in drinking water, platelet and leukocyte recruitment was reduced to ND levels. Increased platelet adhesion was observed in HCD mice receiving platelets from HCD-Los mice, consistent with a direct beneficial action of losartan on the vessel wall. Hypercholesterolemia elicited an oxidative stress in venules and an increased expression of P-selectin and AT1-R. The oxidative stress and AT1-R upregulation were reduced by losartan, but the P-selectin response was not. We propose that AT1-R engagement contributes to the prothrombogenic and proinflammatory state induced in venules by hypercholesterolemia. Key Words: receptors, angiotensin II Ⅲ microcirculation Ⅲ hypercholesterolemia Ⅲ leukocytes I t is well established that angiotensin II (Ang II), the effector component of the renin-angiotensin system, is a potent vasoconstrictor that plays a key role in the maintenance of blood pressure and fluid homeostasis. However, it is becoming increasingly apparent that Ang II also possesses potent proinflammatory properties, such as enhancing reactive oxygen species (ROS) generation, 1 increasing the expression of cell adhesion molecules (CAMs) and stimulating the release of cytokines and chemoattractants such as interleukin (IL)-6, IL-8, and monocyte chemoattractant protein-1. 2-4 Ang II stimulates superoxide release from NAD(P)H oxidase by engaging the high-affinity Ang II type-1 receptor (AT1-R), thereby initiating the phosphorylation of critical enzyme subunits. 5,6 In vitro, Ang II elevates surface expression of CAMs 7 such as vascular CAM-1 (VCAM-1), 8 intercellular adhesion molecule-1 (ICAM-1), 9 and E-selectin. 10 In vivo, superfusion of postcapillary venules with Ang II results in leukocyte recruitment and ROS generation. 11,12 These leukocyte adhesion responses appear to be mediated by a ROSdependent mobilization of preformed P-selectin to the endothelial surface. 11,12 Ang II can act as an immunomodulatory agent that engages the AT1-R to increase the number of Th1 cytokine (interferon-␥)-producing T cells 13 and elevate CD40 expression on circulating monocytes. 14 Ang II may also exert some of its proinflammatory effects through activatio...