The paper concludes that, even for measures that share the highlighted mathematical properties, magnitude comparisons are most usefully assessed relative to an elicited or estimated underlying distribution for the two proportions. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health 2020.Facioscapulohumeral muscular dystrophy (FSHD) is an incurable disorder linked to ectopic expression of DUX4. However, DUX4 is notoriously difficult to detect in FSHD muscle cells, while DUX4 target gene expression is an inconsistent biomarker for FSHD skeletal muscle biopsies, displaying efficacy only on pathologically inflamed samples. Immune gene misregulation occurs in FSHD muscle, with DUX4 target genes enriched for those associated with inflammatory processes. However, there lacks an assessment of the FSHD immune cell transcriptome, and its contribution to gene expression in FSHD muscle biopsies. Here we show that EBV-immortalised FSHD lymphoblastoid cell lines express DUX4 and both early and late DUX4 target genes. Moreover, a biomarker of 237 up-regulated genes derived from FSHD lymphoblastoid cell lines is elevated in FSHD muscle biopsies compared to controls. The FSHD Lymphoblast score is unaltered between FSHD myoblasts/myotubes and their controls though, implying a non-myogenic cell source in muscle biopsies. Indeed, the FSHD Lymphoblast score correlates with the early stages of muscle inflammation identified by histological analysis on muscle biopsies, while our two late DUX4 target gene expression biomarkers associate with macroscopic inflammation detectable via MRI.  https://www.selleckchem.com/products/mavoglurant.html  Thus FSHD lymphoblastoid cell lines express DUX4 and some early and late DUX4 target genes and so muscle-infiltrated immune cells may contribute the molecular landscape of FSHD muscle biopsies. © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For Permissions, please email journals.permissions@oup.com.Endometrial stromal cells differentiate into decidual cells through the process of decidualization. This differentiation is critical for embryo implantation and the successful establishment of pregnancy. Recent epidemiological studies have suggested that thyroid hormone is important in the endometrium during implantation, and it is commonly believed that thyroid hormone is essential for proper development, differentiation, growth, and metabolism. This study aimed to investigate the impact of thyroid hormone on decidualization in human endometrial stromal cells (hESCs) and define its physiological roles in vitro by gene targeting. To identify the expression patterns of thyroid hormone, we performed gene expression profiling of hESCs during decidualization after treating them with the thyroid hormone levothyroxine (LT4). A major increase in decidual response was observed after combined treatment with ovarian steroid hormones and thyroid hormone. Moreover, LT4 treatment also affected the regulation of many transcription factors important for decidualization. We found that type 3 deiodinase, which is particularly important in fetal and placental tissues, was up-regulated during decidualization in the presence of thyroid hormone. Further, it was observed that progesterone receptor, an ovarian steroid hormone receptor, was involved in thyroid hormone-induced decidualization. In the absence of thyroid hormone receptor (TR), due to the simultaneous silencing of TRα and TRβ, thyroid hormone expression was unchanged during decidualization. In summary, we demonstrated that thyroid hormone is essential for decidualization in the endometrium. This is the first in vitro study to find impaired decidualization as a possible cause of infertility in subclinical hypothyroidism (SCH) patients. © Endocrine Society 2020. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.BACKGROUND Sarcopenia is often conceptualized as a precursor to loss of mobility, but its effect on recovery of mobility after a hip fracture is unknown. We determined the prevalence of low muscle strength (weakness) after hip fracture using putative sarcopenia metrics (absolute grip strength, and grip strength normalized to body mass index, total body fat, arm lean mass, and weight) identified by the Sarcopenia Definitions and Outcomes Consortium (SDOC). METHODS We examined two well-characterized hip fracture cohorts of community-dwelling older adults from the Baltimore Hip Studies (BHS). The prevalence of muscle weakness was assessed using the SDOC cut-points compared to published definitions at two and six months post-fracture. We assessed associations of two-month weakness with 6-month walking speed less then 0.6 m/s and calculated the sensitivity and specificity in predicting lack of meaningful change in walking speed (change less then 0.1 m/s) at six months. RESULTS 246 participants (192 women; 54 men) were included; mean (SD) age of 81(8) for women and 78 (7) for men. At two months, 91% women and 78% men exhibited slow walking speed ( less then 0.6 m/s). SDOC grip strength standardized by weight ( less then 0.34 kg women, less then 0.45 kg men) was the most prevalent measure of weakness in men (74%) and women (79%) and provided high sensitivity in men (86%) and women (84%) predicting lack of meaningful change in walking speed at six months, although specificity was poor to moderate. CONCLUSIONS SDOC cut-points for grip strength standardized to weight provided consistent indication of poor walking speed performance post hip fracture. © The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.Myotonic dystrophy type 1 (DM1), the most common adult muscular dystrophy, is an autosomal dominant disorder caused by an expansion of a (CTG)n tract within the 3' untranslated region (3'UTR) of the DMPK (dystrophia myotonica protein kinase) gene. Mutant DMPK mRNAs are toxic, present in nuclear RNA foci and correlated with a plethora of RNA splicing defects. Cardinal features of DM1 are myotonia and cardiac conduction abnormalities. Using transgenic mice, we have demonstrated that expression of the mutant DMPK 3'UTR is sufficient to elicit these features of DM1. Here, using these mice, we present a study of systemic treatment with an antisense oligonucleotide (ASO) (ISIS 486178) targeted to a non-CUG sequence within the 3'UTR of DMPK. RNA foci and DMPK 3'UTR mRNA levels were reduced in both the heart and skeletal muscles. This correlated with improvements in several splicing defects in skeletal and cardiac muscles. The treatment reduced myotonia and this correlated with increased Clcn1 expression. Furthermore, functional testing showed improvements in treadmill running.