探讨降低电磁干扰之道

电磁干扰是电子设备和系统设计当中不能回避的问题.电源是把电子设备和电源网络联系起来的部分,因此电源引起的电磁干扰值得认真关注.随着开关稳压器的广泛使用,它越来越多地存在于电子设备中.目前,减轻电磁干扰的方法很多,包括接地、屏蔽和滤波等方式,本文将着重介绍用多相同步和扩展频谱频率调制(SSFM)的方式来降低电磁干扰.     

Effect of AlN and Al2O3 additions on the phase relationships and morphology of SiC Part I Compositions and properties

X-ray diffraction was utilized to follow the transformation from -SiC (3C) to the various -SiC polytypes in the presence of AlN and Al₂O₃ additives after hot pressing from 1700 to 2100°C. The 2H- and 6H-polytypes of -SiC were the predominate polytypes with additions of only AlN or Al₂O₃, respectively. The amount of 2H- and 6H-polytypes, and subsequently the microstructural morphology of the SiC materials, were found to be controlled by varying the amount of AlN and Al₂O₃. Improvements in fracture toughness to 9 MPa-m were achieved with flexural strengths ranging from 600 to 900 MPa. These results suggest that accurate control of the polytypic make-up of SiC-based materials, along with their mechanical properties, can be achieved through AlN and Al₂O₃ additions.     

High power, 8.5 W CW, visible laser diodes

Visible laser diodes have been fabricated from AlGaInP operating at approximately 680 nm to high output powers. Broad area lasers with 100 mu m wide emitting apertures operate to greater than 1 W CW with a different efficiency of 38%. The threshold current densities of the material have been measured to be as low as 350 A/cm/sup 2/ for lasers with 30% mirror reflectivities. Monolithic bars 8 mm long with 50 mu m emitting apertures periodically spaced on 500 mu m centres have been fabricated which operate to 8.5 W CW.<>     

Correcting temperature-sensitive protein folding defects

Recently, we found that different low molecular weight compounds, all known to stabilize proteins in their native conformation, are effective in correcting the temperature-sensitive protein folding defect associated with the deltaF508 cystic fibrosis transmembrane regulator (CFTR) protein. Here we examined whether the folding of other proteins which exhibit temperature-sensitive folding defects also could be corrected via a similar strategy. Cell lines expressing temperature-sensitive mutants of the tumor suppressor protein p53, the viral oncogene protein pp60src, or a ubiquitin activating enzyme E1, were incubated at the nonpermissive temperature (39.5 degrees C) in the presence of glycerol, trimethylamine N-oxide or deuterated water. In each case, the cells exhibited phenotypes similar to those observed when the cells were incubated at the permissive temperature (32.5 degrees C), indicative that the particular protein folding defect had been corrected. These observations, coupled with our earlier work and much older studies in yeast and bacteria, indicate that protein stabilizing agents are effective in vivo for correcting protein folding abnormalities. We suggest that this type of approach may prove to be useful for correcting certain protein folding abnormalities associated with human diseases.     

In vitro antimycobacterial activity of 5-chloropyrazinamide

5-Chloropyrazinamide and 5-chloropyrazinoic acid were evaluated for in vitro activity against Mycobacterium tuberculosis, Mycobacterium bovis, and several nontuberculous mycobacteria by a broth dilution method. 5-Chloropyrazinamide was more active than pyrazinamide against all organisms tested. It is likely that this agent has a different mechanism of action than pyrazinamide.     

Pathogenesis of oleic acid-induced lung injury in the rat: Distribution of oleic acid during injury and early endothelial cell changes

Oleic acid-induced lung injury, a well-described laboratory model for acute pulmonary injury in the rat and other species, causes morphologic and cellular changes similar to human adult respiratory distress syndrome (ARDS). Experiments were performed to test the hypothesis that the initial event of oleic acid lung injury is damage of the pulmonary vascular endothelium by oleic acid, with subsequent pulmonary damage and inflammation. Oleic acid levels were followed in the lung and other tissues by measuring accumulation of¹⁴C-oleic acid; the direct effects of oleic acid and other fatty acids on rat endothelial cells, alveolar type II cells, and hepatocytes in culture were determined. Lung tissue from treated rats was also examined by light and electron microscopy for evidence of endothelial cell damage. At 30 min after injury, oleic acid reached high concentrations in lung tissue as demonstrated by presence of radiolabel (3.24×10⁻⁶ moles per gram of tissue), with counts in the lung nearly an order of magnitude greater than in any other organ measured. Oleic acid was present in the lung mostly as free fatty acid (85%), and was also present in the alveolar fluid supernatans, rather than being cell-associated (1.7×10⁻⁷ moles vs. 1.1×10⁻⁸ moles at 30 min). Oleic acid was toxic to endothelial cells after one minute of exposure at concentrations of 5×10⁻⁴M and above. Electron microscopy showed endothelial cell changes as early as 10 min after induction of injuryin vivo, including the presence of endothelial cell blebbing. The results of these studies suggest that the initial event in oleic acid lung injury is damage to the pulmonary vascular endothelial cell.     

Positron emission tomography with 2-[18F]Fluoro-2-deoxy-D-glucose and 16alpha-[18F]fluoro-17beta-estradiol in breast cancer: correlation with estrogen receptor status and response to systemic therapy

We assessed the value of positron emission tomography (PET) with 2-[18F]fluoro-2-deoxy-D-glucose (FDG) and 16alpha-[18F]fluoro-17beta-estradiol (FES) in women with breast cancer for predicting response to systemic therapy. Results of FES-PET were correlated with estrogen receptor (ER) status. Forty-three women with locally advanced or metastatic breast cancer underwent FDG-PET and FES-PET prior to institution of systemic therapy. All patients had measurable disease and had tumors submitted for ER determination. Cancers were considered functionally hormone sensitive if the standardized uptake value of the lesion on FES-PET was >/=1.0 (FES+) and hormone resistant if the standardized uptake value was <1.0 (FES-). Information obtained by FES-PET was compared with the results of ER assays. The tumor response to chemotherapy and hormonal therapy was correlated with intensity of uptake by both FDG-PET and FES-PET. The ER status of the breast cancers was negative (ER-) in 20 patients, positive (ER+) in 21 patients, and unknown in 2 patients. All 20 of the ER- tumors were also FES-. However, of the 21 ER+ tumors, 16 were FES+ and 5 were FES-. Thirty patients were treated initially with chemotherapy, and 21 (70%) demonstrated objective responses. We were unable to correlate the response to chemotherapy with information obtained by FDG-PET or FES-PET. Thirteen patients were treated with hormone therapy, and 8 (61%) responded to that therapy. Only 1 of the 5 patients whose tumors were ER+ but FES- received hormone therapy, and this treatment resulted in disease stabilization only. Multiple sites of disease were assessed by FES-PET in 17 patients with metastatic breast cancer. Functional hormone sensitivity, defined by FES-PET, was concordant with multiple lesions in 13 (76%). Ten patients with locally advanced breast cancer developed recurrent disease. The initial site of recurrence was the breast in 5 patients. Of the 5 patients with systemic recurrence, 4 had disease detected at the site of recurrence on the pretreatment FDG-PET study but not detected on pretreatment computed tomography. In our experience, FDG-PET imaging is more sensitive than conventional imaging methods, including computed tomography, in staging women with breast cancer. When compared with the in vitro assay of ER status, FES-PET has an apparent sensitivity of 76% and specificity of 100%. Our finding of a subset of patients who have tumors that are ER+ and FES- suggests that the functional assessment of hormone sensitivity by PET imaging can identify patients with ER+ disease whose tumors are likely to be hormone refractory.     

New words from old: A formalism for word-formation

Many languages make use of word-formation devices to allow speakers or writers to create new words when the existing vocabulary proves inadequate. In this paper we consider how these devices can be expressed formally, allowing them to be used in word- and sentence-generation, for dictionary expansion, and the like. The paper begins with some typical word-formation rules drawn mostly from French. Attention is drawn to some features of these rules which must be captured in any formal representation. The formal representation of a basic lexical transformation is presented in some detail, along with a number of examples. A computer implementation of the transformation system is described, together with a range of applications. A discussion of static and dynamic generation leads to the concept of an inverted transformation.Michael Levison is Professor and Head of the Department of Computing and Information Science at Queen's University at Kingston. His research interests currently centre on natural language generation and editing systems. He has written many articles on computer applications in literary and linguistic studies.Greg Lessard is an Associate Professor in the Department of French Studies at Queen's University. A linguist, his research interests include computational modelling of natural language performance (including second language learner French and linguistic humour) and computer-aided textual analysis (including repeated string and complex textual structures.)