Development of Automated Visual Acuity Measurement Using a Calibration-Free Eye-Tracking System.

Purpose Infant vision assessment often relies on grating acuity; however, its objectivity and convenience must be improved. A calibration-free eye-tracking system, even in preverbal children, enables easy and precise gaze analysis. This pilot study aimed to develop a reliable automated monocular vision screening. Methods Participants (n=118) underwent a grating visual acuity test using the eye-tracking system. Correlations between the grating acuity, uncorrected visual acuity, and refractive error were analyzed across different cutoff values of fixation duration percentage. Results Strong correlations were found between the grating acuity and refractive error at 69% and 88% thresholds. Similar correlations with uncorrected visual acuity were noted at 70% and 89% thresholds. False-negatives around the 70% threshold were noted, indicating potential overestimation of acuity in cases of low visual acuity/high refractive error. Discussion The results highlight the feasibility of calibration-free eye-tracking system-based monocular vision screening with an optimal screening threshold of 90%.

Vasopressin Expressed in Hypothalamic CRF Neurons Causes Impaired Water Diuresis in Secondary Adrenal Insufficiency.

Patients with secondary adrenal insufficiency can present with impaired free water excretion and hyponatremia, which is due to the enhanced secretion of vasopressin (AVP) despite increased total body water. AVP is produced in magnocellular neurons in the paraventricular nucleus of the hypothalamus (PVH) and supraoptic nucleus and in parvocellular corticotropin-releasing factor (CRF) neurons in the PVH. This study aimed to elucidate whether magnocellular AVP neurons or parvocellular CRF neurons coexpressing AVP are responsible for the pathogenesis of hyponatremia in secondary adrenal insufficiency. The number of CRF neurons expressing copeptin, an AVP gene product, was significantly higher in adrenalectomized AVP-floxed mice (AVPfl/fl) than in sham-operated controls. Adrenalectomized AVPfl/fl mice supplemented with aldosterone showed impaired water diuresis under ad libitum access to water or after acute water loading. They became hyponatremic after acute water loading, and it was revealed under such conditions that aquaporin-2 (AQP2) protein levels were increased in the kidney. Furthermore, translocation of AQP2 to the apical membrane was markedly enhanced in renal collecting duct epithelial cells. Remarkably, all these abnormalities observed in the mouse model for secondary adrenal insufficiency were ameliorated in CRF-AVP-/- mice that lacked AVP in CRF neurons. Our study demonstrates that CRF neurons in the PVH are responsible for the pathogenesis of impaired water excretion in secondary adrenal insufficiency.