Computer monitor pixellation and Landolt C visual acuity.

Purpose: To investigate the effects of computer monitor pixel density on Landolt C visual acuity measurements and to provide appropriate pixel density recommendations for Landolt C vision chart design.

Methods: Participants were 10 healthy observers aged 18-31 years (mean 21.7 ± 3.

Deprotection of centromeric cohesin at meiosis II requires APC/C activity but not kinetochore tension.

Genome haploidization involves sequential loss of cohesin from chromosome arms and centromeres during two meiotic divisions. At centromeres, cohesin's Rec8 subunit is protected from separase cleavage at meiosis I and then deprotected to allow its cleavage at meiosis II. Protection of centromeric cohesin by shugoshin-PP2A seems evolutionarily conserved.

Worth 4 Dot App for Determining Size and Depth of Suppression.

Purpose: To describe and evaluate an iOS application suppression test, Worth 4 Dot App (W4DApp), which was designed and developed to assess size and depth of suppression.

Methods: Characteristics of sensory fusion were evaluated in 25 participants (age 12-69 years) with normal (n = 6) and abnormal (n = 19) binocular vision. Suppression zone size and classification of fusion were determined by W4DApp and by flashlight Worth 4 Dot (W4D) responses from 33 cm to 6 m.

Prc1-rich kinetochores are required for error-free acentrosomal spindle bipolarization during meiosis I in mouse oocytes.

Acentrosomal meiosis in oocytes represents a gametogenic challenge, requiring spindle bipolarization without predefined bipolar cues. While much is known about the structures that promote acentrosomal microtubule nucleation, less is known about the structures that mediate spindle bipolarization in mammalian oocytes. Here, we show that in mouse oocytes, kinetochores are required for spindle bipolarization in meiosis I.

Tex19.1 inhibits the N-end rule pathway and maintains acetylated SMC3 cohesin and sister chromatid cohesion in oocytes.

Age-dependent oocyte aneuploidy, a major cause of Down syndrome, is associated with declining sister chromatid cohesion in postnatal oocytes. Here we show that cohesion in postnatal mouse oocytes is regulated by Tex19.1.