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The "5 gauss line" is a phrase that is likely to be familiar to everyone working with MRI, but what is its significance, how was it defined, and what changes are currently in progress? This review explores the history of 5 gauss (0.5 mT) as a threshold for protecting against inadvertently putting cardiac pacemakers, implantable cardioverter defibrillators, and other active implantable medical devices into a "magnet mode." Additionally, it describes the background to the recent change of this threshold to 9 gauss (0.9 mT) in the International Standard IEC 60601‐2‐33 edition 4.0 that defines basic safety requirements for MRI. Practical implications of this change and some ongoing and emerging issues are also discussed. [ABSTRACT FROM AUTHOR]

Aim: To investigate relationships between insulin clearance, insulin secretion, hepatic fat accumulation and insulin sensitivity in black African (BA) and white European (WE) men. Methods: Twenty‐three BA and twenty‐three WE men with normal glucose tolerance, matched for age and body mass index, underwent a hyperglycaemic clamp to measure insulin secretion and clearance, hyperinsulinaemic‐euglycaemic clamp with stable glucose isotope infusion to measure whole‐body and hepatic‐specific insulin sensitivity, and magnetic resonance imaging to quantify intrahepatic lipid (IHL). Results: BA men had higher glucose‐stimulated peripheral insulin levels (48.1 [35.5, 65.2] × 103 vs. 29.9 [23.3, 38.4] × 103 pmol L−1 × min, P =.017) and lower endogeneous insulin clearance (771.6 [227.8] vs. 1381 [534.3] mL m−2 body surface area min −1, P <.001) compared with WE men. There were no ethnic differences in beta‐cell insulin secretion or beta‐cell responsivity to glucose, even after adjustment for prevailing insulin sensitivity. In WE men, endogenous insulin clearance was correlated with whole‐body insulin sensitivity (r = 0.691, P =.001) and inversely correlated with IHL (r = −0.674, P =.001). These associations were not found in BA men. Conclusions: While normally glucose‐tolerant BA men have similar insulin secretory responses to their WE counterparts, they have markedly lower insulin clearance, which does not appear to be explained by either insulin resistance or hepatic fat accumulation. Low insulin clearance may be the primary mechanism of hyperinsulinaemia in populations of African origin. [ABSTRACT FROM AUTHOR]