Ralph Gross | Search PubMed

PubMed2004

Appearance-based face recognition and light-fields.

Arguably the most important decision to be made when developing an object recognition algorithm is selecting the scene measurements or features on which to base the algorithm. In appearance-based object recognition, the features are chosen to be the pixel intensity values in an image of the object. These pixel intensities correspond directly to the radiance of light emitted from the object along certain rays in space. The set of all such radiance values over all possible rays is known as the plenoptic function or light-field. In this paper, we develop a theory of appearance-based object recognition from light-fields. This theory leads directly to an algorithm for face recognition across pose that uses as many images of the face as are available, from one upwards. All of the pixels, whichever image they come from, are treated equally and used to estimate the (eigen) light-field of the object. The eigen light-field is then used as the set of features on which to base recognition, analogously to how the pixel intensities are used in appearance-based face and object recognition.

Algorithms↗

PubMed2004

Streptococcus pneumoniae-induced caspase 6-dependent apoptosis in lung epithelium.

Streptococcus pneumoniae is the major pathogen of community-acquired pneumonia and one of the most common causes of death due to infectious diseases in industrialized countries. Lung epithelium lines the airways and constitutes the first line of innate defense against respiratory pathogens. Little is known about the molecular interaction of pneumococci with lung epithelial cells. Apoptosis of lung epithelium is involved in some bacterial lung infections. In this study different pneumococcal strains specifically induced either apoptotic or necrotic death of human alveolar and bronchial epithelial cells. Pneumococcus-induced apoptosis did not depend on the virulence factors pneumolysin and H(2)O(2). Apoptotic cells showed increased activity of caspases 6, 8, and 9 but not increased activity of caspase 3. Moreover, programmed cell death could be strongly reduced by a caspase 6 inhibitor and a pan-caspase inhibitor. Inhibitors of calpain and chymotrypsin- and trypsin-like proteases also reduced pneumococcus-induced apoptosis. Furthermore, pneumococcus-infected human alveolar epithelial cells showed Bid cleavage and reduced levels of Bcl2 and Bax. Overexpression of Bcl2 in these cells reduced apoptosis significantly. Thus, pneumococci induced apoptosis of human alveolar and bronchial epithelial cells. Programmed cell death was executed by caspase 6 and noncaspase proteases, but not by caspase 3, and could be blocked by overexpression of Bcl2.

Apoptosis↗