When Math Hurts: Math Anxiety Predicts Pain Network Activation in Anticipation of Doing Math

Math can be difficult, and for those with high levels of mathematics-anxiety (HMAs), math is associated with tension, apprehension, and fear. But what underlies the feelings of dread effected by math anxiety? Are HMAs’ feelings about math merely psychological epiphenomena, or is their anxiety grounded in simulation of a concrete, visceral sensation – such as pain – about which they have every right to feel anxious? We show that, when anticipating an upcoming math-task, the higher one’s math anxiety, the more one increases activity in regions associated with visceral threat detection, and often the experience of pain itself (bilateral dorso-posterior insula). Interestingly, this relation was not seen during math performance, suggesting that it is not that math itself hurts; rather, the anticipation of math is painful. Our data suggest that pain network activation underlies the intuition that simply anticipating a dreaded event can feel painful. These results may also provide a potential neural mechanism to explain why HMAs tend to avoid math and math-related situations, which in turn can bias HMAs away from taking math classes or even entire math-related career paths.     

A rapid screening method for hepatocyte nuclear factor 1 alpha frameshift mutations; prevalence in maturity-onset diabetes of the young and late-onset non-insulin dependent diabetes

Non-insulin dependent diabetes (NIDDM) is a polygenic heterogeneous disorder of glucose homeostasis. Maturity-onset diabetes of the young (MODY) is a monogenic subtype of NIDDM characterised by early-onset (< 25 years) and autosomal dominant inheritance. Mutations in the hepatocyte nuclear factor 1 alpha (HNF-1α) gene have recently been shown to cause MODY. The incidence of mutations in this gene in MODY and late-onset NIDDM is not known. We have developed a rapid specific polymerase chain reaction test for HNF-1α mutations; this test involves the use of fluorescently labelled forward primers and modified reverse primers to detect length polymorphisms resulting from frameshift mutations. With this method, we have screened 102 MODY probands, viz. 60 defined according to strict diagnostic criteria (autosomal dominant inheritance and at least one member diagnosed age < 25 years) and 95 late-onset NIDDM probands (diagnosed 35–70 years with ≥ 1 affected relative), for the presence of 9 known HNF-1α frameshift mutations, including 6 that occur at two sites for recurring mutation (residues 291/292 and 379). Mutations were detected in 11 of the strictly defined MODY probands and one mutation was also found in a single subject with early-onset NIDDM but no family history of the disease. The HNF-1α frameshift mutations were not detected in any late-onset NIDDM subjects, suggesting these mutations do not have a major role in the pathogenesis of NIDDM. Our results indicate that the prevalence of the nine frameshift mutations in strictly defined UK MODY is 18%, with the P291fsinsC mutation alone having a frequency of 13%. Received: 13 May 1997 / Accepted: 13 August 1997     

Sur la Production d'Anticorps au Moyen d'Un Antigène Enrobé dans la Lanoline-Vaseline

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