"It's like having a superpower": Reclaiming creativity and the intersectional experiences of trans young adults of color.

Trans young adults of color experience systemic harm that contributes to negative health outcomes and hinders their ability to live freely. The present study used a grounded theory qualitative methodology rooted in a critical-ideological paradigm to understand the intersections of racial and gender oppression. Trans young adults of color from across the United States (N = 15; ages 20-29; majority racial identities: Asian, Black, and multiracial; majority gender identities: nonbinary and transmasculine) participated in a semistructured interview. Analyses identified a six-category empirical framework explaining major dimensions and processes of intersectional experiences of trans people of color. The core category, Reclaiming Creativity, reflected how trans communities of color use creativity to build their identities and communities beyond intersectional oppressive societal norms and imagine a better, more liberated world. The remaining five categories were Creating and Recreating Identity, Experiencing Discrimination and Its Impacts on Wellness, Surviving Oppression and Compromising Authentic Self, Embracing Identity Strengths, and Finding Liberation. They provided insights into the role of creativity within the intersectional experiences of trans young adults of color. In doing so, they provided directions to address structural injustice, pursue liberation, and allow creativity to flourish. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Family rejection and LGBTQ+ Asian Americans' psychological distress and disordered eating: The role of conflicts in allegiances and family shame.

OBJECTIVES: Lesbian, gay, bisexual, trans, and queer (LGBTQ+) Asian Americans experience unique psychological health concerns at the intersection of multiple forms of marginalization. White supremacist, cisheteronormative, and colonial ideals and their structural and interpersonal manifestations may encourage family rejection of LGBTQ+ identities within Asian American family units. Family shame, conflicts in allegiances, and internalized anti-LGBTQ+ stigma were hypothesized as mediators in the association between family rejection and psychological distress and disordered eating. METHOD: The present study examined family rejection and its impacts on psychological distress and disordered eating in a sample of LGBTQ+ Asian American adults (N = 155; Mage = 24.26; 30.3% gender diverse) using a cross-sectional survey design and path analysis. RESULTS: There was a significant serial mediation such that family rejection was positively associated with conflicts in allegiances, family shame, and psychological distress (B = .12, p = .01). The same serial mediation was nonsignificant for disordered eating (B = .04, p = .26). CONCLUSIONS: Results indicate the importance of considering conflicts in allegiances, family shame, and the interpersonal dynamics of LGBTQ+ Asian Americans in understanding experiences of psychological distress and disordered eating. Implications are drawn for further research, clinical work, and broader efforts addressing the larger sociocultural environment that encourages family rejection of LGBTQ+ identity. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Impact of Racist Microaggressions and LGBTQ-Related Minority Stressors: Effects on Psychological Distress Among LGBTQ+ Young People of Color.

BACKGROUND: College students situated at the nexus of racial and sexual and gender minority (SGM) identities may experience multiple identity-related oppressions. We assessed whether racist microaggressions and lesbian, gay, bisexual, transgender, queer, or questioning (LGBTQ)-related minority stressors (ie, family rejection, identity concealment, racialized heterosexism and/or cisgenderism, internalized LGBTQ-phobia, and victimization) are associated with greater psychological distress among SGM college students of color (SOC) (students who identified as Hispanic/Latinx and/or any nonwhite race). METHODS: Participants were a subset of SOC (n = 200) from a larger nonprobability cross-sectional study of SGM college students. Participants were recruited by using online social media platforms and university email listserves from May through August 2020. Participants completed an online Qualtrics survey using previously validated measures of minority stress, racist microaggressions, and psychological distress. Simple and covariate-adjusted multiple linear regression models were used to examine the associations between racist microaggressions and LGBTQ-related minority stressors with psychological distress. RESULTS: In simple linear regression models, racist microaggressions and all LGBTQ-related stressors (ie, family rejection, identity concealment, racialized heterosexism and/or cisgenderism, internalized LGBTQ-phobia, and victimization) were significantly and positively associated with greater psychological distress. In covariate-adjusted multiple linear regression, racist microaggressions, internalized LGBTQ-phobia, and LGBTQ-related family rejection (but not identity concealment, racialized heterosexism and/or cisgenderism, and victimization) were independently and significantly associated with greater psychological distress. CONCLUSION: Study findings reveal that racist microaggressions, along with LGBTQ-related family rejection and internalized LGBTQ-phobia, have a significant impact on psychological distress among SGM SOC. Public health leaders have an important opportunity for policy and program development and reform to address the identity-related mental health needs of SGM SOC.

An intersectional investigation of Asian American men's muscularity-oriented disordered eating: Associations with gendered racism and masculine norms.

Grounded in an intersectional framework, the present study investigated the extent to which racism, gendered racism, and conformity to masculine norms are associated with Asian American men's muscularity-oriented disordered eating. The study also examined if ethnic identity moderated the association between both forms of racism and muscularity-oriented disordered eating. 220 Asian American men completed an online cross-sectional survey that contained the study questionnaires. Hierarchical regression analyses were conducted to examine the associations between our predictor variables and muscularity-oriented disordered eating. Gendered racism, conformity to the masculine norms of playboy, heterosexual presentation and self-reliance were positively associated with muscularity-oriented disordered eating, whereas conformity to power over women was negatively associated. Racism and the remaining masculine norms were not associated with muscularity-oriented disordered eating. Ethnic identity did not moderate the association between either form of racism and muscularity-oriented disordered eating. Given that gendered racism was positively associated with muscularity-oriented disordered eating whereas racism was not, researchers and practitioners may consider prioritizing intersectionality in their understanding of Asian American men's eating pathology. Results emphasize the importance of examining both race and gender in conceptualizing Asian American men's muscularity-oriented disordered eating.Data Availability Statement: Data for this study are available upon request from the first author.

Minority stressors and their associations with severe psychological distress among gender-diverse people.

People whose gender does not align with assigned sex often experience negative mental health outcomes related to cisnormative societal expectations and oppression, including familial rejection, threat of harm, and identity invalidation (e.g., misgendering). This study merged two cross-sectional data sets of trans and gender-diverse people (N = 363; Mage = 22.02) investigating how various types of distal minority stress experiences impact psychological distress. We tested the associations between three minority stressors (i.e., family rejection, threat of harm, and identity invalidation) and psychological distress using unadjusted and adjusted regression models, including gender-stratified models. In the overall unadjusted model, all three stressors were significantly, positively associated with psychological distress, with identity invalidation having the highest standardized ß value. In the adjusted overall model, only identity invalidation was significantly associated with distress. Results varied in gender-stratified models. Additionally, participants who experienced any of the three stressors had predicted mean distress scores at or above the cutoff for severe psychological distress, while those who did not fell below that cutoff. Results highlight the differential impact of minority stress experiences on gender-diverse young adults and provide directions for clinical competency, interventions, and future research toward understanding mental health disparities for trans people. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Comparison of end-tidal carbon monoxide measurements with direct antiglobulin tests in the management of neonatal hyperbilirubinemia.

OBJECTIVE: Determine whether management of neonatal hyperbilirubinemia differs if one used end-tidal carbon monoxide (CO) corrected for ambient CO (ETCOc) measurements instead of direct antiglobulin test (DAT) results to assess the severity of hemolysis. STUDY DESIGN: Retrospective chart review of infants with total bilirubin and ETCOc levels measured from July 2016 to August 2018. The reported treatment is the hypothetical management infants might have received had there been strict adherence to American Academy of Pediatrics guidelines, rather than the actual management they received. RESULT: Only 27.2% of 191 DAT(+) infants were hemolyzing based on ETCOc, while 29.1% of DAT (-) infants were hemolyzing based on ETCOc. Management of 18 (9.4%) infants differed depending if ETCOc or DAT were used to determine hemolysis. Eight fewer infants would have received phototherapy if ETCOc was used. CONCLUSIONS: ETCOc is a more accurate determinant of hemolysis in the newborn, and its use can lead to less phototherapy.

Redox signals and NF-kappaB activation in T cells.

Accumulating data from a number of laboratories have recently indicated that the response of transcription factor NF-kappaB to alterations in the redox homeostasis of cells may play an important role in modulating immune function. The activation of NF-kappaB has been recognized to regulate a number of genes necessary for normal T cell responses including IL-2, IL-6, IL-8, and several T cell surface receptors. Diminished NF-kappaB activity has been shown to occur in T cells with aging, suggesting that impaired activation of NF-kappaB might occur during cellular senescence. In addition, aberrancies in NF-kappaB activity have been implicated in the immunopathogenesis of diseases involving immune or inflammatory processes such as atherosclerosis and HIV-1 infection. The role of H2O2 and other reactive oxygen species (ROS) as an integratory secondary messenger for divergent T cell signals has been complicated by the fact that various T cell lines and peripheral blood T cells differ markedly in the levels of NF-kappaB activation induced by oxidant stress. Additionally, proposed pathways of NF-kappaB activation have been based on indirect evidence provided by experiments which used antioxidants to inhibit active NF-kappaB formation. Further, complete activation of T cells requires at least two signals, one that stimulates an increase in intracellular calcium and one that stimulates enzymatic processes including kinases. Similarly, substantial evidence indicates that full activation of NF-kappaB requires dual signals. The ability of H2O2 or other ROS to induce T cell signals and functional responses by these two mechanisms is reviewed and the specific response of NF-kappaB to redox changes in T cells is examined. Data are also presented to suggest that the redox regulation in NF-kappaB activation may be relevant to immune-related diseases and to aging.

Alterations in the expression of interleukin-2R subunits by activated T cells from elderly humans are uncoupled from aberrancies in G1/S progression.

Activated T cells from elderly humans are known to often display a decline in interleukin-2 (IL-2) production. However, the possible effects of aging on the expression of IL-2 receptor (IL-2R) subunits by human T cells are more controversial and less well characterized. In the present investigation, the surface expression of IL-2Ralpha, IL-2Rbeta, and IL-2Rgamma subunits on resting and activated T cells from 15 sets of elderly and young humans was evaluated. The results showed no significant differences in the average expression of IL-2Ralpha, IL2Rbeta, and IL-2Rgamma on resting T cells from elderly and young subjects, with values of 10% or less. Similarly, no significant differences were found in the mean levels of IL-2Ralpha, IL-2Rbeta, and IL-2Rgamma on T cells from elderly and young subjects stimulated with anti-Ig cross-linked anti-CD3 (monoclonal antibody [mAb] OKT3), phorbol myristate acetate (PMA), anti-CD3 and PMA, or 1% phytohemagglutinin (PHA) plus PMA. Analyses of the expression of IL-2R on activated T cells from elderly people revealed a marked heterogeneity in IL2R levels irrespective of the stimuli. Other experiments showed that the age-related alterations in surface expression of IL-2Ralpha were not correlated to changes in the release of soluble IL-2Ralpha. Age-related changes in IL-2R expression on activated T cells from individual donors were not coupled to the ability of the T cells to undergo G(1)/S progression. Collectively, these observations suggest that activated T cells from elderly people exhibit substantial heterogeneity in the expression of IL-2R subunits and that alterations in IL-2R expression may be distinct from intrinsic defects in G(1)/S progression and proliferative responses.

Evaluation of in vitro activity of quinupristin/dalfopristin and comparator antimicrobial agents against worldwide clinical trial and other laboratory isolates.

This report summarizes the activities of quinupristin/dalfopristin (Q/D) and appropriate comparator antibiotics, including ciprofloxacin, erythromycin, gentamicin, rifampin, teicoplanin, and vancomycin, against selected gram-positive pathogens, including Enterococcus faecium, Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumoniae, Streptococcus agalactiae, and Streptococcus pyogenes. The study pathogens were obtained from 2 sources: (1) clinical isolates taken from patients participating in Q/D worldwide Phase III comparative and noncomparative (emergency-use program) clinical trials; and (2) other isolates collected from the laboratories of 45 geographically distinct medical centers around the world. Q/D was highly active, with minimum inhibitory concentrations (MICs) < or = 1.0 microg/mL against most isolates, including those known to be resistant to methicillin, vancomycin, or erythromycin. Q/D was active (MICs < or = 1 microg/mL) against 95% of the vancomycin-resistant E. faecium strains, for example, whereas ciprofloxacin was active against 6%. Q/D was equally active against methicillin-susceptible or -resistant S. aureus strains (MIC90=1 microg/mL), as was vancomycin (MIC90=2 microg/mL), whereas ciprofloxacin was much less active against methicillin-resistant strains than against methicillin-susceptible strains (MIC90=32 vs 1 microg/mL). Given its spectrum of activity, Q/D may provide a viable option for the treatment of severe respiratory and skin and skin-structure infections caused by gram-positive bacteria, especially when strains with known or suspected resistance to other commonly used antibiotics are present.

Foveal ganglion cell loss is size dependent in experimental glaucoma.

PURPOSE: The purpose of this study was to study the pattern of foveal ganglion cell loss in experimental glaucoma. METHODS: Retinal ganglion cell size and number in the foveal region of seven monkey eyes with experimental glaucoma was determined and compared to normal monkey eyes. Serial sections of macular retina were studied in two regions: the plateau of peak density of ganglion cells (800-1100 microns from the fovea), and within 500 microns of the foveal center. RESULTS: In normal eyes, cell densities were 37,900 +/- 2700 in the foveal plateau and 17,200 +/- 1800 cells/mm2 in the foveal center. There was selective loss of larger ganglion cells in glaucoma eyes. The degree of foveal ganglion cell loss was significantly correlated to the degree of nerve fiber loss in the temporal optic nerve of the same eye. CONCLUSIONS: Detection of early, central visual function loss in glaucoma could be enhanced by testing functions subserved by larger retinal ganglion cells.

Primary open-angle glaucoma is not associated with photoreceptor loss.

PURPOSE: To determine if photoreceptors die in primary open-angle glaucoma. METHODS: Retinas were examined in a masked fashion from nine standard locations of 14 eyes with documented open-angle glaucoma and from nine age-matched control eyes. The number and density of photoreceptors, as well as the area and height of the outer nuclear layer, were calculated with an automated image analysis system. The number of photoreceptors per 0.1 mm of retina was determined. RESULTS: No significant difference was seen between control and glaucomatous eyes in comparisons of photoreceptor density, outer nuclear layer height, or photoreceptors per 0.1 mm of retinal length in nine retinal zones. There was no detectable association between photoreceptor number and severity of glaucoma (defined as mild, moderate, or severe), visual field, and optic nerve fiber loss. In eyes in which damage predominated in the upper or lower visual field, no corresponding difference in photoreceptor number in upper compared to lower retinal zones was observed. CONCLUSION: Photoreceptors are not lost in substantial numbers in primary open-angle glaucoma.

Number of ganglion cells in glaucoma eyes compared with threshold visual field tests in the same persons.

PURPOSE: To compare the number of retinal ganglion cells (RGCs) topographically mapped with specific visual field threshold test data in the same eyes among glaucoma patients. METHODS: Seventeen eyes of 13 persons with well-documented glaucoma histories and Humphrey threshold visual field tests (San Leandro, CA) were obtained from eye banks. RGC number was estimated by histologic counts of retinal sections and by counts of remaining axons in the optic nerves. The locations of the retinal samples corresponded to specific test points in the visual field. The data for glaucoma patients were compared with 17 eyes of 17 persons who were group matched for age, had no ocular history, and had normal eyes by histologic examination. RESULTS: The mean RGC loss for the entire retina averaged 10.2%, indicating that many eyes had early glaucoma damage. RGC body loss averaged 35.7% in eyes with corrected pattern SD probability less than 0.5%. When upper to lower retina RGC counts were compared with their corresponding visual field data within each eye, a 5-dB loss in sensitivity was associated with 25% RGC loss. For individual points that were abnormal at a probability less than 0.5%, the mean RGC loss was 29%. In control eyes, the loss of RGCs with age was estimated as 7205 cells per year in persons between 55 and 95 years of age. In optic nerves from glaucoma subjects, smaller axons were significantly more likely to be present than larger axons (R2 = 0.78, P<0.001). CONCLUSIONS: At least 25% to 35% RGC loss is associated with statistical abnormalities in automated visual field testing. In addition, these data corroborate previous findings that RGCs with larger diameter axons preferentially die in glaucoma.

Obstructed axonal transport of BDNF and its receptor TrkB in experimental glaucoma.

PURPOSE: In both animal model system and in human glaucoma, retinal ganglion cells (RGCs) die by apoptosis. To understand how RGC apoptosis is initiated in these systems, the authors studied RGC neurotrophin transport in experimental glaucoma using acute intraocular pressure (IOP) elevations in rats and chronic IOP elevation and unilateral optic nerve transections in monkeys. METHODS: Eyes were studied in masked fashion by light and electron microscopy and by immunohistochemistry with antibodies directed against the tyrosine kinase receptors (TrkA, B, and C) and against brain-derived neurotrophic factor (BDNF), as well as by autoradiography to identify retrograde axonal transport of 125I-BDNF injected into the superior colliculus. RESULTS: With acute glaucoma in the rat, RGC axons became abnormally dilated, accumulating vesicles presumed to be moving in axonal transport at the optic nerve head. Label for TrkB, but not TrkA, was relatively increased at and behind the optic nerve head with IOP elevation. Abnormal, focal labeling for TrkB and BDNF was identified in axons of monkey optic nerve heads with chronic glaucoma. With acute IOP elevation in rats, radiolabeled BDNF arrived at cells in the RGC layer at less than half the level of control eyes. CONCLUSIONS: Interruption of BDNF retrograde transport and accumulation of TrkB at the optic nerve head in acute and chronic glaucoma models suggest a role for neurotrophin deprivation in the pathogenesis of RGC death in glaucoma.

Retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis.

PURPOSE: To investigate whether retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis. METHODS: Chronic elevated eye pressure was produced in 20 monkey eyes, and the optic nerve was transected unilaterally in the orbit of 10 monkeys and 14 rabbits. Sixteen monkey and 14 rabbit eyes were studied as normal controls. Analytic methods included light and electron microscopy, histochemistry for DNA fragmentation (TUNEL method), and DNA electrophoresis in agarose gels. RESULTS: Dying ganglion cells in the experimental retinas exhibited morphologic features of apoptosis, including chromatin condensation and formation of apoptotic bodies. Cells with a positive reaction for DNA fragmentation were observed in eyes subjected to axotomy and experimental glaucoma but were only rarely encountered in control eyes. No evidence of internucleosomal fragmentation was detected electrophoretically, possibly because of the small proportion of cells that were dying at any given time. CONCLUSION: Some retinal ganglion cells injured by glaucoma and by axotomy die by apoptosis.

Retrograde axonal transport of BDNF in retinal ganglion cells is blocked by acute IOP elevation in rats.

PURPOSE: To determine whether acute experimental glaucoma in rats obstructs retrograde transport of brain-derived neurotrophic factor (BDNF) to retinal ganglion cells (RGCs). METHODS: Forty rats had unilateral injection of either (125)I-BDNF (20 animals) or a mixture of (125)I-BDNF and 100-fold excess nonradiolabeled BDNF (20 animals). In each group of 20 animals, eyes contralateral to injection had either normal intraocular pressure (IOP; 10 animals) or IOP elevated to 25 mm Hg below the systolic blood pressure of the eye (10 animals). In each group of 20 rats, ipsilateral eyes had IOP set at systolic blood pressure (4 eyes), had optic nerve transection (10 eyes), or had normal IOP (6 eyes). Six hours after injection, animals were killed and tissues were fixed, embedded, and sectioned for autoradiography. Grain counts were performed over retina and optic nerve using automated image analysis. RESULTS: IOP elevation to 25 mm Hg below systolic blood pressure (perfusion pressure [PP] 25) decreased median retinal nerve fiber layer (NFL) grains by 38% compared with controls (P: < 0.001). Competition by cold BDNF reduced NFL grains by 28% (P: = 0.013). Considering only the radioactivity representing specific retrograde transport of BDNF, IOP elevation to PP25 reduced transport by 74%, whereas elevation to PP0 (equaling systolic blood pressure) reduced specific transport by 83%. CONCLUSIONS: BDNF is transported retrogradely from the superior colliculus in adult rats, and this transport is substantially inhibited by acute IOP elevation. Deprivation of BDNF among RGCs may contribute to neuron loss in glaucoma.

Optic nerve transection in monkeys may result in secondary degeneration of retinal ganglion cells.

PURPOSE: Interest in neuroprotection for optic neuropathies is, in part, based on the assumption that retinal ganglion cells (RGCs) die, not only as a result of direct (primary) injury, but also indirectly as a result of negative effects from neighboring dying RGCs (secondary degeneration). This experiment was designed to test whether secondary RGC degeneration occurs after orbital optic nerve injury in monkeys. METHODS: The superior one third of the orbital optic nerve on one side was transected in eight cynomolgus monkeys (Macaca fascicularis). Twelve weeks after the partial transection, the number of RGC bodies in the superior and inferior halves of the retina of the experimental and control eyes and the number and diameter of axons in the optic nerve were compared by detailed histomorphometry. Vitreous was obtained for amino acid analysis. A sham operation was performed in three additional monkeys. RESULTS: Transection caused loss of 55% +/- 13% of RGC bodies in the superior retina of experimental compared with fellow control eyes (mean +/- SD, t-test, P < 0.00,001, n = 7). Inferior RGCs, not directly injured by transection, decreased by 22% +/- 10% (P = 0.002). The loss of superior optic nerve axons was 83% +/- 12% (mean +/- SD, t-test, P = 0.0008, n = 5) whereas, the inferior loss was 34% +/- 20% (P = 0.02, n = 5). Intravitreal levels of glutamate and other amino acids in eyes with transected nerves were not different from levels in control eyes 12 weeks after injury. Fundus examination, fluorescein angiography, and histologic evaluation confirmed that there was no vascular compromise to retinal tissues by the transection procedure. CONCLUSIONS: This experiment suggests that primary RGC death due to optic nerve injury is associated with secondary death of surrounding RGCs that are not directly injured.

Immunolocalization of TGF-beta 1, TGF-beta 2, and TGF-beta 3 in the anterior segment of the human eye.

PURPOSE: To determine the distribution of transforming growth factor type beta (TGF-beta) in the anterior segment of the human eye. This knowledge is important because TGF-beta may regulate various physiologic responses in the anterior segment by controlling cell proliferation and differentiation, angiogenesis, and extracellular matrix composition. METHODS: Immunohistochemical methods were used to localize the beta 1, beta 2, and beta 3 isoforms of TGF-beta in the anterior segment of the human eye. RESULTS: Eight of eight eyes (six eye bank specimens and two eyes enucleated because of choroidal melanoma) exhibited staining for at least one of the TGF-beta isoforms. TGF-beta 1 was found in superficial limbal epithelial cells (four of eight eyes) and in the stroma proximal to the ciliary processes (seven of eight eyes). TGF-beta 2 was found in superficial limbal epithelial cells (six of eight eyes), the conjunctival stroma (eight of eight eyes), in the ciliary processes (three of eight eyes), and in a diffuse distribution in the region of the radial and circular muscles of the ciliary body (eight of eight eyes). In addition, TGF-beta 2 was found in the stroma adjacent to the pigmented epithelium in the pars plana (eight of eight eyes). TGF-beta 3 was found in white blood cells in one of eight specimens; otherwise it was not found in the anterior segment. The corneal stroma, corneal endothelium, trabecular meshwork, iris, and ciliary epithelia did not exhibit immunoreactivity with the antibodies used in this study. CONCLUSION: TGF-beta 1 and TGF-beta 2 have a distinct and specific distribution in the anterior segment of the adult human eye.

A clinical study of peripapillary crescents of the optic disc in chronic experimental glaucoma in monkey eyes.

OBJECTIVE: We produced chronic experimental glaucoma in 41 monkey eyes and assessed the long-term effects of elevated intraocular pressure on the presence of, and changes in, peripapillary crescents. METHODS: Three readers independently plotted peripapillary crescent size and location using stereo fundus photographs before and after chronic elevation of intraocular pressure in 41 monkey eyes. RESULTS: Crescents were found in a majority of normal eyes. After chronically elevated intraocular pressure, new peripapillary crescents developed in only two eyes. Using planimetric analysis, crescent size was enlarged in five (22%) of the 23 eyes with preexisting crescents. Preexisting crescents became more apparent without change in size in a majority of eyes (reader A, 15 [68%] of 22 eyes; reader B, 17 [74%] of 23 eyes; and reader C, 13 [68%] of 19 eyes). CONCLUSIONS: We conclude that peripapillary crescents are often present in normal monkey eyes but that they do not often undergo dramatic changes in size with chronic intraocular pressure elevation. The presence of a crescent was not significantly associated with the development of optic disc cup enlargement in the experimental monkey eye.

Global and regional detection of induced optic disc change by digitized image analysis.

OBJECTIVE: To evaluate two new strategies for the detection of optic disc change within individual eyes by digitized image analysis. METHODS: Eleven normal optic discs of 11 monkeys were imaged with a digital imaging system (Topcon Imagenet, Topcon Instrument Corporation of America, Paramus, NJ) at two intraocular pressures (10 and 45 mm Hg). To detect global change in the disc, we compared conventional optic disc parameters with a new optic disc parameter: mean position of the disc. To detect regional change, the 95% confidence interval for change was calculated for each data point and mapped for each disc. RESULTS: Posterior deformation of the disc surface was detected in seven of 11 eyes using conventional parameters and in 10 of 11 eyes using mean position of the disc. Regions of posterior deformation were detected by 95% confidence interval for change mapping in all 11 discs as localized areas of confluent, posteriorly displaced points. CONCLUSIONS: Mean position of the disc outperformed conventional measurements in the detection of global optic disc change. Ninety-five percent confidence interval for change mapping may allow individual data point-based focal and regional analysis of the disc.