Intra-thyroid esophageal duplication cyst: A case report.

BACKGROUND: Esophageal cysts are relatively rare in clinical practice, with most of the literature comprising case reports. Esophageal cysts protruding into the thyroid gland are easily misdiagnosed as thyroid tumors. No such cases have been reported so far. CASE SUMMARY: This article reports the case of a 31-year-old adult male diagnosed with thyroid nodules before admission. The patient underwent left thyroidectomy and isthmusectomy. During the surgery, esophageal cysts were identified in the esophageal muscle and thyroid glands. The pathology results confirmed a nodular goiter combined with esophageal cysts. Postoperatively, the patient developed a neck infection and underwent another operation and broad-spectrum antibiotic treatment for recovery. CONCLUSION: We report the first clinical case of an esophageal cyst located within the thyroid gland that was successfully treated surgically. Esophageal cyst located within the thyroid gland cause difficulties in diagnosis. In the present study, the contents of the esophageal cysts were calcified foci, and a small amount of fluid mixture, which were easily misdiagnosed as thyroid nodules and misled the surgical methods.

Potentiation of NMDA-Mediated Responses by Amyloid-ß Peptide 1-40 in Rat Sympathetic Preganglionic Neurons.

The abnormal accumulation of amyloid-ß peptides (Aß) is one of the main characteristics of Alzheimer's disease (AD). Cerebro- and cardiovascular diseases may be the risk factors for developing AD. The effect of Aß on central sympathetic control of cardiovascular function remains unclear. The present study examines the acute effects of Aß oligomers on the function of NMDA receptors, a subtype of ionotropic glutamate receptors, in rat sympathetic preganglionic neurons (SPNs). In the in vitro electrophysiological study, Aß1-40 but not Aß1-42 applied by superfusion for 5 min significantly potentiated NMDA-induced depolarizations in SPNs of neonatal rat spinal cord slice preparation. Application of Aß1-40 had little effects on AMPA-induced depolarizations or GABA-induced hyperpolarizations. Treatment with a selective protein kinase C (PKC) inhibitor applied together with Aß1-40 blocked the augmentation by Aß1-40 of NMDA-induced depolarizations. Western blot analysis showed an increase in the levels of phosphoserine 896, selectively regulated by PKC, without significant changes in phosphoserine 897 on GluN1 subunits in lateral horn areas of spinal cord slices following treatment with Aß1-40. In the in vivo study, intrathecal injection of Aß1-40 (0.2 nmol) potentiated the pressor effects induced by NMDA (2 nmol) injected intrathecally in urethane-anesthetized rats. These results suggest that different fragments of Aß may have differential effects on the NMDA receptor function and the selective augmentation of NMDA receptor function by Aß1-40 may involve PKC-dependent mechanisms in sympathetic preganglionic neurons.