ABSTRACT
Trace fear conditioning is characterized by a stimulus-free trace interval (TI) between the conditioned stimulus (CS) and the unconditioned stimulus (US), which requires an array of brain structures to support the formation and storage of associative memory. The entorhinal cortex (EC) has been proposed to provide essential neural code for resolving temporal discontinuity in conjunction with the hippocampus. However, how the CS and TI are encoded at the neuronal level in the EC is not clear. In Exp. 1, we tested the effect of bilateral pre-training electrolytic lesions of EC on trace vs. delay fear conditioning using rats as subjects. We found that the lesions impaired the acquisition of trace but not delay fear conditioning confirming that EC is a critical brain area for trace fear memory formation. In Exp. 2, single-unit activities from EC were recorded during the pretraining baseline and post-training retention sessions following trace or delay conditioning. The recording results showed that a significant proportion of the EC neurons modulated their firing during TI after the trace conditioning, but not after the delay fear conditioning. Further analysis revealed that the majority of modulated units decreased the firing rate during the TI or the CS. Taken together, these results suggest that EC critically contributes to trace fear conditioning by modulating neuronal activity during the TI to facilitate the association between the CS and US across a temporal gap.
ABSTRACT
Rupture of the interventricular septum is a serious complication of acute myocardial infarction, accounting for 5% of death due to acute myocardial infarction. The mortality with medical therapy alone exceeds 90%. Accurate diagnosis, urgent management, and early operative correction are necessary for survival. We report cases of 3 patients with ventricular septal rupture after acute myocardial infarction.
Subject(s)
Humans , Diagnosis , Mortality , Myocardial Infarction , Rupture , Ventricular Septal RuptureABSTRACT
Cardiac metastases of renal cell carcinomas are rare, and usually clinically silent. A case of a 53-year-old man without a significant medical history, who presented with ventricular tachycardia, which resulted in a cardiac mass of the right ventricle is reported. On chest X-ray, echocardiography, CT scanning, esophagogastroduode-noscopy and MRI, multiple metastatic masses were observed in both lungs, and the kidneys, adrenal, stomach and right ventricle. The kidney mass and the gastric polyp were revealed on biopsy to be a renal cell carcinoma mixed with sarcomatoid and conventional types.