Flat-panel CT versus 128-slice CT in temporal bone imaging: Assessment of image quality and radiation dose.

OBJECTIVE: We compared the image quality and radiation dose of flat-panel CT (FPCT) and multi-slice CT (MSCT) performed respectively with an angiographic unit and a 128-slice CT scanner. We investigated whether the higher spatial resolution of FPCT translated into higher image quality and we sought to eliminate inter-subject variability by scanning temporal bone specimens with both techniques. MATERIALS AND METHODS: Fifteen temporal bone specimens were imaged with FPCT and MSCT. Two neuroradiologists experienced in otoradiology evaluated 30 anatomical structures with a 0-2 score; 18 structures important from a clinical perspective were assigned a twofold value in calculation of the overall score. The radiation dose was calculated through the use of an anthropomorphic phantom. RESULTS: The image quality was significantly higher for FPCT than MSCT for 10 of the 30 anatomical structures; the overall score was also significantly higher for FPCT (p = 0.001). The equivalent dose of the two techniques was very similar, but with different effective doses to the organs. CONCLUSION: FPCT performed on an angiographic unit provides higher image quality in temporal bone assessment compared to MSCT performed on a 128-slice CT scanner thanks to its higher spatial resolution, with comparable equivalent doses but different effective doses to the organs.

Lung anatomy, energy load, and ventilator-induced lung injury.

BACKGROUND: High tidal volume can cause ventilator-induced lung injury (VILI), but positive end-expiratory pressure (PEEP) is thought to be protective. We aimed to find the volumetric VILI threshold and see whether PEEP is protective per se or indirectly. METHODS: In 76 pigs (22 ± 2 kg), we examined the lower and upper limits (30.9-59.7 mL/kg) of inspiratory capacity by computed tomography (CT) scan at 45 cmH2O pressure. The pigs underwent a 54-h mechanical ventilation with a global strain ((tidal volume (dynamic) + PEEP volume (static))/functional residual capacity) from 0.45 to 5.56. The dynamic strain ranged from 18 to 100 % of global strain. Twenty-nine pigs were ventilated with end-inspiratory volumes below the lower limit of inspiratory capacity (group "Below"), 38 within (group "Within"), and 9 above (group "Above"). VILI was defined as death and/or increased lung weight. RESULTS: "Below" pigs did not develop VILI; "Within" pigs developed lung edema, and 52 % died before the end of the experiment. The amount of edema was significantly related to dynamic strain (edema 188-153 × dynamic strain, R (2) = 0.48, p < 0.0001). In the "Above" group, 66 % of the pigs rapidly died but lung weight did not increase significantly. In pigs ventilated with similar tidal volume adding PEEP significantly increased mortality. CONCLUSIONS: The threshold for VILI is the lower limit of inspiratory capacity. Below this threshold, VILI does not occur. Within these limits, severe/lethal VILI occurs depending on the dynamic component. Above inspiratory capacity stress at rupture may occur. In healthy lungs, PEEP is protective only if associated with a reduced tidal volume; otherwise, it has no effect or is harmful.

Sclerosing angiomatoid nodular transformation (SANT): report of 25 cases of a distinctive benign splenic lesion.

Twenty-five cases of a morphologically distinctive vascular lesion of the spleen are described. The patients were 17 women and 8 men, ranging in age from 22 to 74 years (mean, 48.4 years; median, 56 years). The most common presentations were incidental finding of an asymptomatic splenic mass (13 patients), abdominal pain or discomfort (6 patients), and splenomegaly (4 patients). None of the patients had evidence of recurrent disease after splenectomy. The splenic lesion was solitary, measuring 3 to 17 cm, and sharply demarcated from the surrounding parenchyma. The cut surface revealed a mass of coalescing red-brown nodules embedded in a dense fibrous stroma. All cases showed a remarkably consistent multinodular appearance at low-power examination. The individual nodules had an angiomatoid appearance, in the sense that they were composed of slit-like, round or irregular-shaped vascular spaces lined by plump endothelial cells and interspersed by a population of spindly or ovoid cells. Some of the nodules (particularly the smaller ones) were surrounded by concentric rings of collagen fibers. Numerous red blood cells were present, as well as scattered inflammatory cells. Nuclear atypia was minimal, mitotic figures were extremely rare, and necrosis was consistently absent. The internodular stroma consisted of variably myxoid to dense fibrous tissue with scattered plump myofibroblasts, plasma cells, lymphocytes, and siderophages. Immunostaining revealed 3 distinct types of vessels in the angiomatoid nodules: CD34+/CD8-/CD31+ capillaries, CD34-/CD8+/CD31+ sinusoids, and CD34-/CD8-/CD31+ small veins, recapitulating the composition of the normal splenic red pulp. These features are therefore different from those of littoral cell angioma, conventional hemangioma, and hemangioendothelioma of the spleen. We interpret these angiomatoid nodules as altered red pulp tissue that had been entrapped by a nonneoplastic stromal proliferative process. The characteristic morphologic appearance, immunophenotype, and benign clinical course suggest that this is a distinctive nonneoplastic vascular lesion of the spleen that we propose to designate as sclerosing angiomatoid nodular transformation (SANT).

Combined typical carcinoid and acinic cell tumor of the lung: a heretofore unreported occurrence.

We report a primary combined typical carcinoid and acinic tumor of the lung in a 70-year-old man. Although a similar case was reported previously, to the best of our knowledge this is the first case in which the diagnosis is supported by both immunohistochemical and ultrastructural findings. We review the literature and discuss the implications of this finding.

Development of resistance to a trinuclear platinum complex in ovarian carcinoma cells.

BBR3464 is a trinuclear platinum complex that exhibits a potent cytotoxicity and efficacy against cisplatin-resistant tumors. To better understand the determinants of cellular resistance to BBR3464, we selected a resistant ovarian carcinoma cell line after exposure to the complex. The resistant cells (A2780/BBR3464) exhibited a high level of resistance to the selecting agent, but a marginal cross-resistance to cisplatin. Although cellular accumulation of BBR3464 was similar in parental and in resistant cells, DNA platination was decreased in A2780/BBR3464 cells, suggesting a reduced drug accessibility to DNA. This behavior reflected a partial drug inactivation at cytoplasmic level, as a consequence of increased levels of nucleophilic molecules including metallothioneins and human neurofilament low, but not glutathione. A2780/BBR3464 cells also exhibited a reduced susceptibility to apoptosis, which was consistent with reduced expression of Bax, and an alteration of DNA mismatch repair system, as reflected by lack of expression of MLH1 and PMS2, which could impair the recognition/repair of DNA lesions. Whereas both platinum drugs induced G2/M arrest in the parental cells, BBR3464, but not cisplatin, caused a late G1 arrest of resistant cells. Cisplatin induced an appreciable increase of p21(WAF1) levels in both models, in contrast to BBR3464 that produced a substantial upregulation of p21(WAF1) only in parental cells. An inverse relationship with p21(WAF1) modulation was found for CHK1 in parental cells treated with both agents and in resistant cells treated with cisplatin. This pattern of response is consistent with a regulatory loop involving p53 and p21(WAF1) at G2 checkpoint. In contrast, no modulation of CHK1 was found in A2780/BBR3464 treated with the triplatinum compound. These findings, indicating a different activation of regulatory pathways at DNA damage checkpoints in response to cisplatin and BBR3464, support an altered ability of resistant cells to recognize or tolerate sublethal lesions induced by BBR3464.

Electron microscopy analysis of early localization of cisplatin in ovarian carcinoma cells.

Taking advantage of the electron-dense nature of platinum, in this study the authors used an electron microscopy approach to investigate the cellular localization of cisplatin in an ovarian carcinoma cell line. Platinum spots were detected in contact with the plasma membrane and the nuclear envelope as well as in the cytoplasm and nuclear matrices. Contact with the plasma membrane was through a single blunt contact or spanning through the membrane. No sequestration in intracellular vescicles was observed, thereby supporting that phagocytosis and receptor-mediated endocytosis were not occurring. A molecular analysis indicated lack of expression of aquaporin 9, thus excluding its involvement in the membrane translocation of cisplatin. The present data suggest that cisplatin rapidly accumulates in the cell through endocytosis-independent membrane translocation and are consistent with passive diffusion.