Inflammatory myofibroblastic tumors include a diverse group of lesions characterized by inflammatory cell infiltration and variable fibrotic responses. Occurrence in the temporal bone is unusual. We ...present CT and MR imaging findings of an inflammatory myofibroblastic tumor of the temporal bone in a 26-year-old patient with repeated paroxystic episodes of rotatory vertigo that occurred over a few days. CT and MR imaging revealed a homogeneously enhancing soft-tissue mass of the right mastoid with bone erosion of the tegmen and extensive dural thickening. The mass resembled a malignant tumor, and the patient underwent an extended mastoidectomy through a retroauricular approach. Microscopic examination showed myofibroblastic spindle cells with mixed inflammatory infiltrate, and the pathologic diagnosis was inflammatory myofibroblastic tumor.
We demonstrate for the first time the efficient mechanical-electrical conversion properties of InGaN/GaN nanowires (NWs). Using an atomic force microscope equipped with a modified Resiscope module, ...we analyse the piezoelectric energy generation of GaN NWs and demonstrate an important enhancement when integrating in their volume a thick In-rich InGaN insertion. The piezoelectric response of InGaN/GaN NWs can be tuned as a function of the InGaN insertion thickness and position in the NW volume. The energy harvesting is favoured by the presence of a PtSi/GaN Schottky diode which allows to efficiently collect the piezo-charges generated by InGaN/GaN NWs. Average output voltages up to 330 ± 70 mV and a maximum value of 470 mV per NW has been measured for nanostructures integrating 70 nm-thick InGaN insertion capped with a thin GaN top layer. This latter value establishes an increase of about 35% of the piezo-conversion capacity in comparison with binary p-doped GaN NWs. Based on the measured output signals, we estimate that one layer of dense InGaN/GaN-based NW can generate a maximum output power density of about 3.3 W/cm². These results settle the new state-of-the-art for piezo-generation from GaN-based NWs and offer a promising perspective for extending the performances of the piezoelectric sources.
Cocaine-induced lesions may cause extensive destruction of the osteocartilaginous structures of the nose, sinuses, and palate that mimics the clinical picture of other diseases.
From January 1991 to ...September 2001 25 patients with cocaine-induced midline destructive lesions were observed at the Department of Otorhinolaryngology of the University of Brescia. The diagnosis was based on physical and endoscopic evaluation, routine blood and urine analysis, radiological findings, and repeated biopsies of the nasal mucosa. Serum was analyzed by the antineutrophilic cytoplasmic antibody (ANCA) test using indirect immunofluorescence and by enzyme-linked immunosorbent assay for antibodies against proteinase 3 and myeloperoxidase.
Septal perforation was present in all 25 patients, 16 of which (68%) also had partial destruction of the inferior turbinate. Hard palate reabsorption was observed in only six patients (24%); in two of these patients, the lesion also extended to the soft palate. Fourteen patients (56%) were positive by the immunofluorescence test (nine patients had a P-ANCA and five patients a C-ANCA pattern). Four patients (16%) with the P-ANCA pattern and all patients with the C-ANCA pattern also tested positive for anti-proteinase 3 antibodies.
Any sinonasal inflammation involving the midline that persists or remains refractory to treatment may be the first manifestation of potentially lethal drug addiction. Cocaine abuse should be considered in the differential diagnosis of destructive lesions of the nasal cavity even in the presence of a positive ANCA test.
A threatening occurrence in some cocaine abusers is the progressive destruction of nasal structures (cocaine-induced midline destructive lesions CIMDL) that may end in a highly severe disease.
Thirty ...patients with CIMDL, 10 healthy patients, 10 patients affected by nasal polyposis, and 10 patients affected by Wegener granulomatosis were observed. Biopsy specimens of nasal mucosa were analyzed by immunohistochemistry for caspases-3, -9 and -8 and by the terminal deoxynucleotidyl transferase-mediated dUTP-digoxygenin nick end labeling (TUNEL) method. The time and concentration-dependent effects of cocaine in vitro were studied in HaCat cells by TUNEL and Western blotting.
All CIMDL biopsy specimens showed abundant caspase-3 and caspase-9 expression but no caspase-8 positive cells. No obvious expression of any caspases was detected in biopsy specimens from healthy subjects or in patients affected by nasal polyposis or Wegener granulomatosis. In HaCat cells cellular changes were observed, which confirmed induction of massive apoptotic events. The rate of apoptosis in HaCat cells was dependent on the concentration of cocaine. After 1 hour, 2.5, 5, and 10 mM of cocaine induced 16, 45, and 84% of apoptotic figures, respectively, while 6 hours of exposure increased apoptosis to 25, 54, and 94% at the same concentrations. Caspase expression and activation in HaCat cells treated with 100 microM and 1 mM of cocaine for 1 hour were confirmed by Western blotting.
Cultured epithelial cells show both time- and dose-dependent increases in apoptosis and cellular damage on cocaine treatment. We suggest that some abusers trigger CIMDL by abnormally boosting apoptosis within nasal epithelial cells. Cocaine abusers with higher apoptotic rates may predict whether they will eventually develop CIMDL.
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