Background: Optic neuritis is an inflammatory demyelinating condition of the optic nerve that causes subacute visual loss. It is often the result of an underlying systemic condition, such as multiple sclerosis. Due to the possible long-term morbidity associated with this condition, it is essential that the emergency physician recognizes the diagnosis and expedites treatment.
View Article and Find Full Text PDFLung sonography has rapidly emerged as a reliable technique in the evaluation of various thoracic diseases. One important, well-established application is the diagnosis of a pneumothorax. Prompt and accurate diagnosis of a pneumothorax in the management of a critical patient can prevent the progression into a life-threatening situation.
View Article and Find Full Text PDFGenetic research aimed at understanding human health and disease is grounded in the study of genetic variation. The inclusion of research subjects with diverse ancestral backgrounds is essential for genetic and genomic research that fully explores human diversity. Large-scale cohort studies and biobanks in Europe and the United States often do not include the breadth of ethnic and racial diversity observed in their countries' citizens.
View Article and Find Full Text PDFObjective: Loss to follow-up threatens internal and external validity yet little research has examined ways to limit participant attrition. We conducted a systematic review of studies with a primary focus on strategies to retain participants in health care research.
Study Design And Settings: We completed searches of PubMed, CINAHL, CENTRAL, Cochrane Methodology Register, and EMBASE (August 2005).
Mice genetically engineered to lack complex gangliosides are improved hosts for raising antibodies against those gangliosides. We report the generation and characterization of nine immunoglobulin G (IgG)-class monoclonal antibodies (mAbs) raised against the four major brain gangliosides in mammals. These include (designated as ganglioside specificity-IgG subclass) two anti-GM1 mAbs (GM1-1, GM1-2b), three anti-GD1a mAbs (GD1a-1, GD1a-2a, GD1a-2b), one anti-GD1b mAb (GD1b-1), and three anti-GT1b mAbs (GT1b-1, GT1b-2a, GT1b-2b).
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