Hodgkin disease: contributions of chest CT in the initial staging evaluation

Chest radiographs and chest computed tomography (CT) scans were compared in 203 patients with newly diagnosed Hodgkin disease. The incidence of positive findings was tabulated from six intrathoracic lymph node groups, lung parenchyma, pericardium, pleura, and chest wall. The discordant cases were assessed to determine impact on clinical management. The CT scans provided additional evidence of disease involvement, ranging from 0% to 15% at each of the designated anatomic sites. Treatment was altered in 9.4% of all patients (19 of 203), including 13.8% (nine of 65) of those undergoing radiation therapy alone and 8.2% (ten of 122) of those undergoing combined-modality treatment. We conclude that routine chest CT examinations are valuable in the clinical management of those patients for whom radiation therapy is planned.     

The use of deep inspiration preceding the valsalva maneuver and rapid expiration in color doppler imaging of the lower extremity veins

Deep inspiration preceding Valsalva maneuver and rapid expiration immediately following it (DIVE) enhance venous blood flow on color Doppler flow imaging (CDI). The effect of DIVE was assessed in 115 consecutive lower extremity examinations. Of these, 95 or 115 (83%) had negative CDI sonograms, and 20 of 115 (17%) had partially (six of 115) or completely (14 of 115) occluding deep vein thrombosis. DIVE enhanced venous blood flow in 68% of the negative cases, resulting in transient venous distention, and/or more complete color filling, and/or greater spectral flow velocities. The 14 cases with completely occluding thrombi showed no response to DIVE. Six cases with partially occluding thrombi showed moderate to mild response to DIVE, with improved color delineation of the residual patent lumen around the thrombus. The authors conclude that DIVE facilitates deep venous CDI, especially when compression cannot be used to augment venous flow.     

Lethal encephalitis in myeloid differentiation factor 88-deficient mice infected with herpes simplex virus 1

Herpes simplex virus 1 (HSV-1), a large DNA virus from the Herpesviridae family, is the major cause of sporadic lethal encephalitis and blindness in humans. Recent studies have shown the importance of Toll-like receptors (TLRs) in the immune response to HSV-1 infection. Myeloid differentiation factor 88 (MyD88) is a critical adaptor protein that is downstream to mediated TLR activation and is essential for the production of inflammatory cytokines. Here, we studied the relationship between MyD88 and HSV-1 using a purified HSV-1 isolated from a natural oral recurrent human infection. We observed the activation of TLR-2 by HSV-1 in vitro using Chinese hamster ovary cells stably transfected with a reporter gene. Interestingly, we found that only peritoneal macrophages from MyD88-/- mice, but not macrophages from TRL2-/- or from wild-type mice, were unable to produce tumor necrosis factor-alpha in response to HSV-1 exposure. Additionally, although TLR2-/- mice showed no enhanced susceptibility to intranasal infection with HSV-1, MyD88-/- mice were highly susceptible to infection and displayed viral migration to the brain, severe neuropathological signs of encephalitis, and 100% mortality by day 10 after infection. Together, our results suggest that innate resistance to HSV-1 is mediated by MyD88 and may rely on activation of multiple TLRs.