Biomedical subjects

Robin Ray

Publications and source records attributed to Robin Ray.

3 recordsLinked to original sources

PubMed2005

Evaluation of image artifact produced by optical coherence tomography of retinal pathology.

PURPOSE: To determine the frequency and type of optical coherence tomography (OCT) fast macular thickness map (FMTM) scan artifacts, and whether these artifacts depend on patient diagnosis, demographics, and ocular therapy. DESIGN: Retrospective observational case series. METHODS: Records from patients who underwent an ophthalmologic evaluation by a member of the Duke University Eye Center vitreoretinal faculty and had an OCT scan produced by the FMTM protocol between July 7, 2003 and July 31, 2003 were reviewed. The relationships between OCT scan artifacts and ocular diagnosis, ocular treatment, and patient demographics were determined. Logistic regression was used to relate OCT scan artifacts simultaneously with ocular diagnosis and treatment. RESULTS: Scans from 171 eyes were analyzed. Retinal scan artifacts, though not observed in normal eyes, were identified frequently in eyes with macular pathology (P = .049). Artifacts were observed in 43.2% of all scans, and of these, an erroneous retinal thickness measurement was obtained in 62.2%. Six types of OCT surface map artifacts were observed. Of these, inner and outer retinal misidentification, degraded image artifact, and "off center" artifact were significantly associated with central thickness calculation errors (P < .001). Neovascular age-related macular degeneration (AMD), full-thickness macular hole, and photodynamic therapy were all associated with increased artifact (P = .002, .022, and <.001, respectively). CONCLUSION: Optical coherence tomography scan artifacts are seen surprisingly frequently, adversely affect retinal thickness measurements in a high proportion of cases, and are diagnosis-dependent. Recognition of these artifacts will improve retinal thickness measurement accuracy, and will prevent faulty treatment decisions that are based on inaccurate retinal thickness measurements.

Aged↗

PubMed2005

NADPH oxidase and endothelial cell function.

Intracellular ROS (reactive oxygen species) such as superoxide and H2O2 have been increasingly appreciated to have a role in endothelial pathophysiology. Of the several sources within the vasculature, a family of multi-subunit NADPH oxidases appears to be a predominant contributor of endothelial superoxide. More importantly, this enzyme system is activated by numerous stimuli and is involved in triggering diverse intracellular signalling pathways ('redox-sensitive' signalling pathways) that have a central role in conditions such as endothelial activation and inflammation, cell growth, apoptosis and hypertrophy. Furthermore, NADPH oxidase-derived superoxide contributes to the impairment of endothelium-dependent vasodilatation by inactivating nitric oxide; the resultant endothelial dysfunction is implicated in the pathophysiology of diseases such as atherosclerosis, hypertension, diabetic vasculopathy and heart failure. A detailed understanding of the regulation of NADPH oxidases and their modulation and downstream effects may define novel therapeutic targets for cardiovascular disease prevention and treatment in the clinical setting, in contrast with global antioxidant therapy which has to date been disappointing.

Cardiovascular Diseases↗

PubMedDate not supplied

NADPH oxidases in cardiovascular health and disease.

Increased oxidative stress plays an important role in the pathophysiology of cardiovascular diseases such as hypertension, atherosclerosis, diabetes, cardiac hypertrophy, heart failure, and ischemia-reperfusion. Although several sources of reactive oxygen species (ROS) may be involved, a family of NADPH oxidases appears to be especially important for redox signaling and may be amenable to specific therapeutic targeting. These include the prototypic Nox2 isoform-based NADPH oxidase, which was first characterized in neutrophils, as well as other NADPH oxidases such as Nox1 and Nox4. These Nox isoforms are expressed in a cell- and tissue-specific fashion, are subject to independent activation and regulation, and may subserve distinct functions. This article reviews the potential roles of NADPH oxidases in both cardiovascular physiological processes (such as the regulation of vascular tone and oxygen sensing) and pathophysiological processes such as endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, angiogenesis, and vascular and cardiac remodeling. The complexity of regulation of NADPH oxidases in these conditions may provide the possibility of targeted therapeutic manipulation in a cell-, tissue- and/or pathway-specific manner at appropriate points in the disease process.

Animals↗