Autoantibodies to cortactin and agrin in sera of patients with myasthenia gravis.

Autoantibodies against agrin and cortactin have been described in patients with myasthenia gravis. To further validate and characterize these autoantibodies, sera and/or plasma exchange material of 135 patients with myasthenia gravis were screened for anti-agrin or anti-cortactin autoantibodies. Autoantibodies against cortactin were detected in three patients and two controls and could be confirmed by cell-based assays using cortactin-transfected human embryonic kidney cells in both controls and one patient, but were not detectable in follow-up sera of the three patients. We did not detect any autoantibodies against agrin. The clinical phenotype of anti-cortactin-positive patients varied, arguing against a relevant pathogenic role.

Combining cortactin and CTTN detection with clinicopathologic features increases effectiveness of survival predictions for patients with resectable hepatocellular carcinoma.

BACKGROUND: Cortactin is an important regulator involved in invasion and migration of tumor cells. Although the relationship between cortactin and tumor invasion has been reported, it lacks follow-up evidence to support the forecasting role of cortactin for HCC prognosis. The aim of this study was to determine whether cortactin detection combined with clinicopathologic features predicts the prognosis efficaciously. METHODS: 91 resectable HCCs were grouped according to clinicopathologic characteristics, and immunohistochemical (IHC) cortactin tumor tissue expression was evaluated. Cortactin gene (CTTN) mRNA of 77 HCCs, as well as that of 20 normal liver tissues, was examined by real-time PCR. Kaplan-Meier method was used for survival analysis. RESULTS: It was found that cortactin expression was associated with liver capsule integrity, cancer embolus in portal vein or distant neoplasm metastasis, and with TNM stage. (p < 0.01) Moreover, CTTN mRNA expression level was higher in high invasiveness group. But no statistical significance was found between low invasiveness and normal control groups. Combining cortactin and CTTN mRNA detection with clinicopathologic features improved the predictive power. High expression of both cortactin and CTTN indicated poor survival time of 12 +/- 3.67 months and low expression indicated longer median survival time of 65 +/- 6.62 months. CONCLUSIONS: These results demonstrate for the first time that cortactin overexpression indicates highly invasive potentialities and poor prognoses with HCCs. Further, the results also suggest that this new accurate evaluating method may be more useful to survival prediction and, therefore, the clinical decision making for resectable

Sex differences in the regulation of cocaine and amphetamine-regulated transcript expression in hypothalamic nuclei of rats by forced swim stress.

Cocaine and amphetamine-regulated transcript (CART) peptides are suggested to play a role in several physiological processes including feeding, reward, neuroendocrine modulation, and the stress response. Although some studies implicate the modulation of CART peptide expression by glucocorticoids, direct evidence relating CART to the stress response is limited. The present study was undertaken to evaluate the possible involvement of CART peptides during acute stress in male and female rats. Forced swim was used as the stress procedure. Following stress, serum adrenocorticotropic hormone (ACTH), and corticosterone (CORT) levels were determined, and CART immunocytochemistry was performed in the paraventricular (PVN) and arcuate (ARC) nuclei of the hypothalamus. Our results depict the following changes: (1) Serum ACTH and CORT levels were increased by stress and CORT levels were higher in female rats than males. (2) Stress modulated the number of CART expressing neurons. The degree and direction of this modulation varied according to the hypothalamic region and the sex of the subject. Forced swim stress increased CART peptide expression significantly in the PVN of female rats. In males, although there was a tendency for an increase in CART-immunoreactive cells by forced swim stress, the difference was not statistically significant. In the ARC nucleus, forced swim stress did not affect CART peptide expression in either sex. Our results suggest differential and sexually dimorphic modulation of CART expression in the PVN and ARC by forced swim stress.