Perceptions of readiness for independent practice among graduating orthopedic surgery residents in Ontario in the last 30 years.

Background: There is increasing concern regarding the lack of physicians and underresourcing of the medical system in Canada. The training of orthopedic surgeons has emerged as an area of particular concern. The purpose of this study was to gain insight into the outcomes of graduates of orthopedic surgery residency programs in Ontario in the last 30 years.

The response to single-gene duplication implicates translation as a key vulnerability in aneuploid yeast.

Aneuploidy produces myriad consequences in health and disease, yet models of the deleterious effects of chromosome amplification are still widely debated. To distinguish the molecular determinants of aneuploidy stress, we measured the effects of duplicating individual genes in cells with different chromosome duplications, in wild-type cells (SSD1+) and cells sensitized to aneuploidy by deletion of RNA-binding protein Ssd1 (ssd1Δ). We identified gene duplications that are nearly neutral in wild-type euploid cells but significantly deleterious in euploids lacking SSD1 or in SSD1+ aneuploid cells with different chromosome duplications.

The visual experience dataset: Over 200 recorded hours of integrated eye movement, odometry, and egocentric video.

We introduce the Visual Experience Dataset (VEDB), a compilation of more than 240 hours of egocentric video combined with gaze- and head-tracking data that offer an unprecedented view of the visual world as experienced by human observers. The dataset consists of 717 sessions, recorded by 56 observers ranging from 7 to 46 years of age. This article outlines the data collection, processing, and labeling protocols undertaken to ensure a representative sample and discusses the potential sources of error or bias within the dataset.

Premature aging in aneuploid yeast is caused in part by aneuploidy-induced defects in Ribosome Quality Control.

Premature aging is a hallmark of Down syndrome, caused by trisomy of human chromosome 21, but the reason is unclear and difficult to study in humans. We used an aneuploid model in wild yeast to show that chromosome amplification disrupts nutrient-induced cell-cycle arrest, quiescence entry, and healthy aging, across genetic backgrounds and amplified chromosomes. We discovered that these defects are due in part to aneuploidy-induced dysfunction in Ribosome Quality Control (RQC).