In veterinary medicine, abdominal ultrasonography is used to rank the differential diagnosis of renal lesions. However, a conventional sonographic examination may show nonspecific findings. The purpose of this study was to assess the computed tomography (CT) findings of canine renal tumors, including renal cell carcinoma (RCC), lymphoma, and hemangiosarcoma (HSA). In this retrospective study, the following CT parameters were recorded for each dog: 1) extent of renal involvement of tumors, 2) enhancement pattern, 3) number of renal tumors, 4) renal tumor vessel enhancement in the corticomedullary phase, 5) presence of lymphadenopathy and lung metastasis, and 6) attenuation values of the renal tumors on the pre- and post-contrast corticomedullary, nephrographic, and excretory phase images. Fifteen dogs met the inclusion criteria, of which nine had RCCs, four had lymphomas, and two had HSAs. RCCs tended to show heterogeneous enhancement and unilateral renal involvement, and vessel enhancement was detected in the corticomedullary phase in dogs with RCC. Conversely, renal lymphomas showed homogeneous enhancement, bilateral renal involvement, and multiple masses; in these dogs, no vessel enhancement was detected in the corticomedullary phase, and the incidence of lymphadenopathy was low. However, in dogs with lymphadenopathy, the renal lymphoma was associated with regionally severe lymphadenopathy. Finally, renal HSAs tended to show heterogeneous enhancement with a non-enhanced area and unilateral renal involvement; in these dogs, vessel enhancement was detected in the nephrographic phase, with the enhancement expanding around the vessel. These findings had no significant differences. Further studies with a larger sample size are required to examine the association between CT and histopathological findings.

In the development of atherosclerosis, inflammatory cells adhere to and migrate into the vascular walls by interacting with vascular smooth muscle cells. To investigate the mechanism of aspirin's anti‐atherogenic activity, we examined whether aspirin inhibits the adhesion of lymphocytes to human aortic smooth muscle cells (AoSMC). Aspirin inhibited T‐cell adhesion to AoSMC activated by interleukin 1β (IL‐1β) in a dose‐dependent manner. Antibodies to the adhesion molecules ICAM‐1 or VCAM‐1, but not to E‐selectin, prevented T‐cell adhesion. ICAM‐1 and VCAM‐1 expression stimulated by IL‐1β was reduced by the treatment with aspirin, whereas the expression of E‐selectin was unaffected. Nuclear factor κB (NF‐κB) activity was enhanced by IL‐1β and reduced by aspirin, indicating that decreased ICAM‐1 and VCAM‐1 expression was due to reduced NF‐κB activity.Thus, aspirin inhibits the adhesion of Jurkat T cells to IL‐1β‐activated AoSMC by reducing NF‐κB activity and decreasing expression of ICAM‐1 and VCAM‐1, and may prevent the development of atherosclerosis.