RESUMEN
We investigated the relations between self-reported math anxiety, task difficulty, and pupil dilation in adults and very young children during math tasks of varying difficulty levels. While task difficulty significantly influenced pupillary responses in both groups, the association between self-reported math anxiety and pupil dilation differed across age cohorts. The children exhibited resilience to the effects of math anxiety, hinting at additional influential factors such as formal math education experiences shaping their relations to mathematics and their impact on cognitive processes over time. Contrary to expectations, no significant association between self-reported math anxiety and pupil dilation during task anticipation was found in either group. In adults, math anxiety influenced pupil dilation exclusively during the initial phase of task processing indicating heightened cognitive load, but this influence diminished during sustained task processing. Theoretical implications emphasize the need for exploring individual differences, cognitive strategies, and the developmental trajectory of math anxiety in very young children.
Asunto(s)
Ansiedad , Matemática , Pupila , Humanos , Femenino , Masculino , Ansiedad/psicología , Pupila/fisiología , Adulto , Niño , Adulto Joven , Cognición/fisiología , PreescolarRESUMEN
BACKGROUND: Maturity-onset diabetes of the young comprises a large group of autosomal inherited gene mutations. Maturity-onset diabetes of the young subtype 5 is caused by mutations in the HNF1B gene. This gene is expressed in the early phase of embryonic development in the pancreas, kidneys, liver, and genital tract; therefore, kidney or urinary tract malformations are associated with diabetes mellitus. The 17q12 deletion syndrome is a cause of maturity-onset diabetes of the young subtype 5 that should be considered. CASE PRESENTATION: We present the case of a 35-year-old Hispanic female patient with a history of bicornuate uterus and polycystic renal disease that required kidney transplant. She had insulin-dependent diabetes, with her mother, maternal grandmother, and great-grandmother showing a similar clinical manifestation. Molecular analysis showed a deletion in chromosome 17q12 involving 15 genes, including HNF1B. Therefore, a diagnosis of deletion syndrome was made. CONCLUSIONS: The 17q12 deletion syndrome represents a rare genetic syndrome that involves different genes, including HNF1B. Principally, it is characterized by the combination of genitourinary tract malformations and diabetes mellitus, similar to our patient.