12 research outputs found
Stereoscopic Cinema and the Origins of 3-D Film, 1838-1952
Though it may come as a surprise to both cinema lovers and industry professionals who believe that 3-D film was born in the early 1950s, stereoscopic cinema actually began in 1838. It occurred more than 100 years before the 3-D boom in Hollywood, which was created by the release of Arch Oboler\u27s African adventure film, âBwana Devilâ. This book not only discusses technological innovation and its cultural context, but also examines the aesthetic aspects of stereoscopic cinema in its first century of production. It also writes a new chapter in the history of early cinema.https://uknowledge.uky.edu/upk_film_and_media_studies/1031/thumbnail.jp
3-D Revolution: The History of Modern Stereoscopic Cinema
3-D Revolution: The History of Modern Stereoscopic Cinema traces the rise of modern 3-D technology from Arch Obolerâs Bwana Devil, the 1952 film that launched the 1950s 3-D boom in Hollywood, to James Cameronâs Avatar, the 2009 release that confirmed 3D film as an enduring part of theatrical entertainment. A comprehensive approach examines the technology for production and exhibition of 3D films and investigates the business, culture, and aesthetics of the genre.https://uknowledge.uky.edu/upk_film_and_media_studies/1035/thumbnail.jp
Cutaneous IgA Deposits in Bullous Diseases Function as Ligands to Mediate Adherence of Activated Neutrophils
Linear IgA bullous dermatosis and dermatitis herpetiformis are inflammatory subepidermal blistering diseases characterized by IgA deposits at the cutaneous epithelial basement membrane and in dermal papillae, respectively. Inflammation in both disorders localizes to sites of IgA deposition and is characterized by a predominance of neutrophils. From these observations we postulate that IgA deposits in both diseases may contribute to the recruitment and/or localization of neutrophils. In this study we examined the ability of in vitro and in vivo bound IgA anti-basement membrane autoantibodies from patients with linear IgA builbus dermatosis and in vivo bound IgA deposits in dermal papillae from patients with dermatitis herpetiformis to mediate adherence of neutrophils stimulated by granulocyte macrophage colony-stimulating factor. The study showed that stimulated neutrophils adhered to basement membranes and dermal papillae containing IgA deposits. Adherence was IgA anti-basement membrane antibody concentration dependent and correlated with the immunofluorescence staining intensity of IgA deposits in dermal papillae. Adherence to IgA deposits but not IgG deposits could be inhibited by purified exogenous secretory IgA but not IgG and adherence to IgG deposits could be inhibited by purified exogenous IgG but not secretory IgA. These results provide direct experimental evidence that cutaneous IgA deposits in linear IgA bullous dermatosis and dermatitis herpetiformis can function as ligands for neutrophil adherence and have a role in the localization of inflammation in these disorders
Cutaneous IgA Deposits in Bullous Diseases Function as Ligands to Mediate Adherence of Activated Neutrophils
Linear IgA bullous dermatosis and dermatitis herpetiformis are inflammatory subepidermal blistering diseases characterized by IgA deposits at the cutaneous epithelial basement membrane and in dermal papillae, respectively. Inflammation in both disorders localizes to sites of IgA deposition and is characterized by a predominance of neutrophils. From these observations we postulate that IgA deposits in both diseases may contribute to the recruitment and/or localization of neutrophils. In this study we examined the ability of in vitro and in vivo bound IgA anti-basement membrane autoantibodies from patients with linear IgA builbus dermatosis and in vivo bound IgA deposits in dermal papillae from patients with dermatitis herpetiformis to mediate adherence of neutrophils stimulated by granulocyte macrophage colony-stimulating factor. The study showed that stimulated neutrophils adhered to basement membranes and dermal papillae containing IgA deposits. Adherence was IgA anti-basement membrane antibody concentration dependent and correlated with the immunofluorescence staining intensity of IgA deposits in dermal papillae. Adherence to IgA deposits but not IgG deposits could be inhibited by purified exogenous secretory IgA but not IgG and adherence to IgG deposits could be inhibited by purified exogenous IgG but not secretory IgA. These results provide direct experimental evidence that cutaneous IgA deposits in linear IgA bullous dermatosis and dermatitis herpetiformis can function as ligands for neutrophil adherence and have a role in the localization of inflammation in these disorders