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In the article, the author discusses the issue of racism in medicine, particularly in palliative care in the U.S., by citing her experiences in helping refugees from Nepal and Bhutan in settling into their home in the U.S. In her experiences, she advocated for effective pain management to refugees with serious medical conditions. Also mentioned is the need to reflect on the racism experienced by African Americans in the U.S. for centuries.

Background: With each stride, galloping horses generate large skeletal loads which influence bone physiology, and may contribute to musculoskeletal injury. Horse speed and stride characteristics are related, but the usefulness of using horse speed and distance travelled as a proxy for stride characteristics is unknown. Objectives: We aimed to determine stride characteristics, their variance and their relationship with speed in horses performing maximally. Study design: Retrospective cross‐sectional analysis of archived data. Methods: Stride characteristics obtained using GPS and inertial sensors in Thoroughbred horses were retrieved. Data per 200 m race segment ('sectionals') for horses competing in races (N = 25,259 race starts) were analysed to determine if speed predicted stride parameters. Multivariable mixed‐effects linear regression models were fitted. Results: Mean (±SD) stride length, stride count (number of strides per 200 m), duration and speed were 7.08 ± 0.39 m, 28.32 ± 1.56 strides/200 m, 0.43 ± 0.02 s/stride and 16.63 ± 1.04 m/s across all sectionals and starts. Speed and stride length decreased, and stride count increased with race progression (P < 0.001). Male sex, greater race distance, better finishing position and firmer track surfaces were associated with less strides per 200 m and longer stride durations. Main limitations: Lack of an independent party validation of the measurement system used in this study. Conclusions: There was a substantial inter‐horse variation in stride parameters, with speed predicting half or less of this variation. Speed alone does not fully explain stride characteristics in horses. Future studies aimed at investigating the impact of gait on bone biology and pathology would benefit from accounting for stride characteristics (eg length and duration). [ABSTRACT FROM AUTHOR]

Background: As myosin heavy chain (MyHC) profile of muscle fibres is heavily influenced by neural input, changes in MyHC expression are expected in horses clinically affected with recurrent laryngeal neuropathy (RLN) yet, this has not been thoroughly investigated. Objectives: To describe the changes in MyHC and fibre diameter in left cricoarytenoideus dorsalis (L‐CAD) muscle of horses with clinical signs of RLN. Study design: Observational cohort study. Methods: Immunohistochemistry was used to assess the MyHC‐based fibre‐type proportion, size and grouping in the L‐CAD of 10 Thoroughbred horses, five clinically affected with RLN and five unaffected controls based on resting endoscopic examination. The Mann‐Whitney U test was used to compare the two groups. Results: Compared to controls (of mean age 3.0 ± 1.7 years) which only expressed type I, IIA and IIX MyHC, the L‐CAD of affected horses (of mean age 2.8 ± 0.8 years) had obvious fibre‐type grouping, and despite apparent compensatory hypertrophy of a small number of fibres, a decrease in overall fibre diameter (median difference −35.2 µm, 95% CI −47.4 to −7.9, P =.02) and diameter of type IIA fibres (median difference −46.8 µm, 95% CI −52.1 to −5.0, P =.03) was observed. Anti‐fast MyHC (MY32) cross‐immunoreacted with embryonic‐MyHC. Whereas MY32‐positive fibres were identified as type IIX in controls, in affected horses these fibres were less than 50 µm diameter with internal nuclei and were MYH3‐positive for embryonic myosin indicating depletion of type IIX fibres, yet active regeneration and fibre renewal. Main limitations: Small sample size that did not include subclinical cases. Fibre size and appearance rather than staining colour were relied upon to differentiate embryonic from type IIX MyHC. Conclusions: Horses clinically affected with RLN have overall atrophy of fibres, loss of IIX fibres and expression of embryonic myosin indicating regenerative capacity. Despite hypertrophy of some remaining fibres, the overall decline in the bulk of fibres, including those most fatigue‐resistant, may be the critical change that results in failure to maintain arytenoid abduction during exercise although direct comparison to subclinical cases is needed to confirm this. [ABSTRACT FROM AUTHOR]