Involvement of MAP Kinases in Apoptosis of Macrophage Treated with Trichomonas vaginalis

A primitive protozoan parasite Trichomonas vaginalis selectively activates the signal transduction pathways in macrophages (RAW264.7). This study evaluated the correlation of these signaling pathways and T. vaginalis-induced cell apoptosis. In macrophages infected with T. vaginalis, apoptosis was assessed on the basis of DNA fragmentation on agarose gel electrophoresis. Infection of macrophages with T. vaginalis induced tyrosine phosphorylation of several proteins. Infected cells with T. vaginalis were shown to associate with phosphorylation of the extracellular signal-regulated (ERK) 1/2 kinase, p38, c-Jun N-terminal kinase (JNK) mitogen-activated protein (MAP) kinases on Western blot analysis. The present finding also demonstrated a link between the ERK1/2, JNK and p38 apoptotic pathways that was modulated by T. vaginalis infection.

Degenerative Changes of Femoral Articular Cartilage in the Knee: Comparative Study of Specimen Sonography and Pathology

PURPOSE: To determine the sonographic findings of degenerative change in femoral articular cartilage of the knee by comparative study of specimen sonography and pathology. MATERIALS AND METHODS: We obtained 40 specimens of cartilage of the femur (20 medial and 20 lateral condylar) from 20 patients with osteoarthritis of the knee who had undergone total knee replacement. The specimens were placed in a saline-filled container and sonography was performed using a 10MHz linear transducer. Sonographic abnormalities were evaluated at the cartilage surface, within the cartilage, and at the bone-cartilage interface, and were compared with the corresponding pathologic findings. In addition, cartilage thickness was measured at a representative portion of each femoral cartilage specimen and was compared with the thickness determined by sonography. RESULTS: 'Dot 'lesions, irregularity or loss of the hyperechoic line, were demonstrated by sonography at the saline-cartilage interface of 14 cartilages. Pathologic examination showed that these findings corresponded to cleft, detachment, erosion, and degeneration. Irregularities in the hyperechoic line at the bone-cartilage interface were revealed by sonography in eight cartilages and were related to irregularity or loss of tidemark, downward displacement of the cartilage, and subchondral callus formation. Dot lesions, corresponding to cleft and degeneration, were noted within one cartilage. Cartilage thickness measured on specimen and by sonography showed no significant difference (p=0.446). CONCLUSION: Specimen sonography suggested that articular cartilage underwent degenerative histopathological change. Cartilage thickness measured by sonography exactly reflected real thickness.

Plain Chest Radiographic Findings of Smoke Inhalation

PURPOSE: To evaluate the plain chest radiographic findings of smoke inhalation. MATERIALS AND METHODS:Our study included 72 burn patients who had suffered smoke inhalation. On admis-sion,all underwent serial portable chest AP radiography. We retrospectively reviewed the plain chest radi-ographs taken between admission and pootburn day five, evaluating the pattern, distribution, and time onset of direct injury to the respiratory system by smoke inhalation. The lesions were also assessed for change. RESULTS: In 16 of 72 patients (22%), abnormal findings of direct injury to the respiratory system by smoke in-halation were revealed by the radiographs. Abnormal findings were 15 pulmonary lesions and one subglottic tracheal narrowing. Findings of pulmonary lesions were multiple small patchy consolidations (10/15), peri-bronchial cuffing (8/15), and perivascular fuzziness (6/15). Patterns of pulmonary lesions were mixed alveolar and interstitial lesion (n=9), interstitial lesion (n=5), and alveolar lesion (n=1). No interlobular septal thicken-ing was observed. Pulmonary edema was distributed predominantly in the upper lung zone and perihilar re-gion, with asymmetricity. Its time of onset was within 24 hours in 13 cases, 24 -48 hours in two cases, and 48 -72 hours in one. Five of 16 patients progressed to ARDS. CONCLUSION: Chest radiographs showed that pulmonary lesions caused by inhalation injury were due to pul-monary edema, which the pattern of which was commonly mixed alveolar and interstitial.

The Radiographic Spectrum of Pulmonary Complications in Major Burn Patient

In recent years, improved antibiotic care and physiologic fluid replacement in cases involving burn wounds have led to a decrease in the rate of fatalaties caused by wound sepsis and shock. There has, however, been an upsurge and relative increase in the frequency (15 -25%) and mortality rate (50 -89 %) of pulmonary complications. Since pulmonary lesions may result from direct injury to the respiratory tract caused by smoke inhalation, from circulatory, metabolic or infectious complications in cases involving cutaneous burns, or may develop during the therapeutic management of these lesions, a wide spectrum of pulmonary abnormalities can occur during the post-burn period. There is considerable overlap between their radiographic appearances, which are often nonspecific. Since the successful management of these patients is based on the early recognition and vig-orous treatment of lesions, familiarity with all facets of these complications, based on a pathophysiology of the injury and on the knowledge of the clinical setting, enables radiologists to make more specific diagnoses.