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The social significance of imitation is that it provides internal tools for understanding the actions of others by simulating or forming internal representations of these actions. Imitation plays a central role in human social behavior by mediating diverse forms of social learning. However, imitation and simulation ability in schizophrenia has not been adequately addressed. The major aim of the present study was to investigate imitation ability in schizophrenia patients and healthy individuals by examining simple motor imitation that involved the replication of meaningless manual and oral gestures, and the imitation of emotional facial expressions, which has implications for mentalizing. A secondary aim of the present study was to investigate the relationships among imitation ability, social functioning, and working memory. Subjects were asked to mimic hand gestures, mouth movements, and facial expressions of others, online. Clinical symptoms, social competence, and working memory were also assessed. Patients with schizophrenia were significantly impaired on all imitation tasks. Imitation errors were significantly correlated with reduced social competence and increased negative symptoms. However, imitation ability was only weakly associated with working memory. To summarize, the present study examined the ability of patients with schizophrenia to imitate the behaviors demonstrated by others. The results indicate a fundamental impairment in imitation ability in schizophrenia and implicate a possible difficulty in simulation. Further research to determine the neural and developmental origins of this difficulty could be extremely helpful in elucidating the role of simulation in schizophrenia and to establish the complex relationships among mental representation, imitation, and social cognition.
Variations in the calpain-10 gene (CAPN10) have been identified among Mexican-Americans, and an at-risk haplotype combination (112/121) defined by three polymorphisms, UCSNP-43, -19, and -63, confers increased risk of type 2 diabetes. Here we examine the three polymorphisms in 1,594 Scandinavian subjects, including 409 type 2 diabetic patients, 200 glucose-tolerant control subjects, 322 young healthy subjects, 206 glucose-tolerant offspring of diabetic patients, and 457 glucose-tolerant 70-year-old men. The frequency of the 112/121 combination was not significantly different in 409 type 2 diabetic subjects compared with 200 glucose-tolerant control subjects (0.06 vs. 0.05; odds ratio 1.32 [95% CI 0.58-3.30]). In glucose-tolerant subjects, neither the single-nucleotide polymorphisms individually nor the 112/121 combination were associated with alterations in plasma glucose, serum insulin, or serum C-peptide levels at fasting or during an oral glucose tolerance test, estimates of insulin sensitivity, or glucose-induced insulin secretion. In conclusion, the frequency of the 112/121 at-risk haplotype of CAPN10 is low among Scandinavians and we were unable to demonstrate significant associations between the CAPN10 variants and type 2 diabetes, insulin resistance, or impaired insulin secretion.