Introduction Peak muscle power is an important determinant of athletic performance across the lifespan that declines with age ( 1 ) and is accompanied by a precipitous decline in serum testosterone ( 2 ). Both present a noteworthy impediment
P Herbert, LD Hayes, NF Sculthorpe, and FM Grace
Yang Lv, Xu Han, Chunyan Zhang, Yuan Fang, Ning Pu, Yuan Ji, Dansong Wang, Xu Xuefeng, and Wenhui Lou
20% or mitotic rate greater than 20 per 10 high power fields. The measurement of analyte Serum values of CgA were measured using an enzyme-linked immunosorbent assay kit (IMRA, CisBio Bioassays Inc., France) according to protocol as the
Kim Magaly Pabst, Robert Seifert, Nader Hirmas, Martina Broecker-Preuss, Manuel Weber, Wolfgang Peter Fendler, Timo Bartel, Sarah Theurer, Ken Herrmann, and Rainer Görges
Key points At a follow-up of >10 years, a single stimulated Tg measurement (maximum 24 months after last radioiodine therapy) seems to have a high predictive power for RFS. At a follow-up >10 years, a single highly sensitive measured
Sofia S Pereira, Tiago Morais, Madalena M Costa, Mariana P Monteiro, and Duarte Pignatelli
functioning and nonfunctioning carcinomas due to the small number of cases in these subgroups, which resulted in a lack of statistical power. According to the ROC curve analysis, the accuracy of StAR as a marker for the differential diagnosis between ACCs and
Ashley K Clift, Omar Faiz, Robert Goldin, John Martin, Harpreet Wasan, Marc-Olaf Liedke, Erik Schloericke, Anna Malczewska, Guido Rindi, Mark Kidd, Irvin M Modlin, and Andrea Frilling
predictive power, in which a C-index greater than 0.5 suggests good predictive ability), in addition to utilising receiver-operating characteristic (ROC) analyses based on survival at 5 and 10 years; the area under the curve (AUC) was calculated for each
Florian Schederecker, Alexander Cecil, Cornelia Prehn, Jana Nano, Wolfgang Koenig, Jerzy Adamski, Tanja Zeller, Annette Peters, and Barbara Thorand
women. Additionally, future well-powered population-based studies should further investigate cause-specific mortality risk. Supplementary materials This is linked to the online version of the paper at https://doi.org/10.1530/EC-20
Manon Engels, Paul N Span, Rod T Mitchell, Joop J T M Heuvel, Monica A Marijnissen-van Zanten, Antonius E van Herwaarden, Christina A Hulsbergen-van de Kaa, Egbert Oosterwijk, Nike M Stikkelbroeck, Lee B Smith, Fred C G J Sweep, and Hedi L Claahsen-van der Grinten
Testicular adrenal rest tumours (TARTs) are benign adrenal-like testicular tumours that frequently occur in male patients with congenital adrenal hyperplasia. Recently, GATA transcription factors have been linked to the development of TARTs in mice. The aim of our study was to determine GATA expression in human TARTs and other steroidogenic tissues. We determined GATA expression in TARTs (n = 16), Leydig cell tumours (LCTs; n = 7), adrenal (foetal (n = 6) + adult (n = 10)) and testis (foetal (n = 13) + adult (n = 8)). We found testis-like GATA4, and adrenal-like GATA3 and GATA6 gene expressions by qPCR in human TARTs, indicating mixed testicular and adrenal characteristics of TARTs. Currently, no marker is available to discriminate TARTs from LCTs, leading to misdiagnosis and incorrect treatment. GATA3 and GATA6 mRNAs exhibited excellent discriminative power (area under the curve of 0.908 and 0.816, respectively), while immunohistochemistry did not. GATA genes contain several CREB-binding sites and incubation with 0.1 mM dibutyryl cAMP for 4 h stimulated GATA3, GATA4 and GATA6 expressions in a human foetal testis cell line (hs181.tes). Incubation of adrenocortical cells (H295RA) with ACTH, however, did not induce GATA expression in vitro. Although ACTH did not dysregulate GATA expression in the only human ACTH-sensitive in vitro model available, our results do suggest that aberrant expression of GATA transcription factors in human TARTs might be involved in TART formation.
Franca Genest, Michael Schneider, Andreas Zehnder, Dominik Lieberoth-Leden, and Lothar Seefried
Aging and concurrent constitutional changes as sarcopenia, osteoporosis and obesity are associated with progressive functional decline. Coincidence and mutual interference of this risk factors require further evaluation.
Cross-sectional evaluation of musculoskeletal health in a community-dwelling cohort of men aged 65–90 years. Objectives included descriptive analysis of age-related decline in physical performance, prevalence of osteoporosis (FRAX-Score), sarcopenia (EWGSOP criteria) and obesity (BMI > 30 kg/m2) and their coincidence/interference.
Based on 507 participants assessed, aging was associated with progressive functional deterioration, regarding power (chair rise test −1.54% per year), performance (usual gait speed −1.38% per year) and muscle force (grip strength −1.52% per year) while muscle mass declined only marginally (skeletal muscle index −0.29% per year). Prevalence of osteoporosis was 41.8% (n = 212) while only 22.9% (n = 116) of the participants met the criteria for sarcopenia and 23.7% (n = 120) were obese. Osteosarcopenia was found in n = 79 (15.6%), sarcopenic obesity was present in 14 men (2.8%). A combination of all three conditions could be confirmed in n = 8 (1.6%). There was an inverse correlation of BMI with physical performance whereas osteoporosis and sarcopenia did not interfere with functional outcomes.
Based on current definitions, there is considerable overlap in the prevalence of osteoporosis and sarcopenia, while obesity appears to be a distinct problem. Functional decline appears to be associated with obesity rather than osteoporosis or sarcopenia. It remains to be determined to what extend obesity itself causes performance deficits or if obesity is merely an indicator of insufficient activity eventually predisposing to functional decline.
Patricia Arroyo Tardio, Gabriela Baldini, and Eleonora Seelig
Objective: Hypercortisolism is a risk factor for obesity. Cortisol increases in response to food intake in lean subjects. In obese subjects, disturbances of the food-induced cortisol peak were reported, but data from sufficiently powered and well-controlled trials are lacking. Understanding the cortisol response to food is essential as amplified, or recurrent cortisol surges could lead to hypercortisolism and contribute to obesity. Therefore, we investigate the cortisol response to food in lean and obese subjects.
Design: This is a non-randomized, open-label study.
Methods: We assessed serum cortisol values after a high-calorie meal in lean and obese male subjects. Cortisol levels were frequently assessed before and for 3 hours after food intake.
Results: 36 subjects (18 lean, 18 obese) were included. There was no difference in overall cortisol levels between both groups during the study (area under the curve (AUC) obese: 55409 ±16994, lean: 60334 ±18001, p=0.4). Total cortisol levels reached peak concentrations 20 minutes after food intake in both groups; the maximum cortisol increase was similar in both groups (cortisol increase obese: 69.6 ±135.5 nmol/l, lean: 134.7 ±99.7 nmol/l; p=0.1). There was no correlation between body mass index (BMI) and baseline cortisol values (R2=0.001, p=0.83), cortisol increase (R2= 0.05, p=0.17), or cortisol AUC (R2= 0.03, p=0.28).
Conclusions: This study demonstrates that high-calorie food intake causes an immediate and substantial cortisol response in lean and obese subjects and is independent of body weight.
Till Ittermann, Rehman Mehmood Khattak, Marcello R P Markus, Jens-Peter Kühn, Marie-Luise Kromrey, Giovanni Targher, Antje Steveling, Matthias Nauck, and Henry Völzke
were transformed by the Royston–Sauerbrei power transformation ( 17 ), which is a linear transformation of the variables into a range between 0.2 and 1. All regression models were weighted for non-response to liver MRI examination. For this, inverse