Outcomes After Aortic Valve Replacement for Asymptomatic Severe Aortic Regurgitation and Normal Ejection Fraction

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A case of cystadenocarcinoma of the liver

A case of cystadenocarcinoma of the liver is reported. The patient was a 73-year-old woman in whom a tumor was detected in the lateral segment of the liver during a health examination. Ultrasonograms and computed tomograms showed a multilocular cystic mass. Magnetic resonance imaging (MRI) showed a multilocular lowintensity mass, including a high-intensity portion and a portal branch compressed by the tumor. MRI with gadolinium showed an enhanced cyst wall. The cystic part of the tumor became smaller and the solid part became larger over a 1-month period, indicating that the tumor was malignant. Subsegmentectomy (S₃) was performed and cystadenocarcinoma with cystadenoma was diagnosed by histopathological examination. Identification of changes in the appearance of a tumor should be helpful for the differential diagnosis of cystadenoma and cystadenocarcinoma.     

Neurogenic stress ulceration caused by laparotomy under anesthesia plus restraint. The device of a new rat model

We report herein, a new method devised of producing neurogenic stress ulceration in rats. An experimental subarachnoid hemorrhage (SAH) was produced in rats by injecting 0.2 ml of arterial blood from other rats into the cisterna magna. Three days later, the rats were laparotomized for 1 hour under ether anesthesia, followed by restraint for 3 hours in wakefulness. The SAH rats were found to develop stress ulcers (UL-I) in the glandular stomach, which were significantly (p less than 0.001) more marked than those in non-SAH rats. Measurements were performed on gastric acid secretion, an important aggressive factor. It was found that the SAH rats undergoing the laparotomy-restraint stress showed a more marked increase in gastric acid secretion and a more marked reduction in MBF, than the non-SAH rats. The effects of bilateral vagotomy, upper abdominal sympathectomy and bilateral adrenalectomy were examined, and it was revealed that the SAH rats were under the condition of hyperreactivity both in the sympathetic and parasympathetic systems and, on this basis, the laparotomy-restraint stress caused the stress gastric ulceration. In this rat model, the laparotomy stress was applied under anesthesia and any exposure to low temperatures which may have interfered with blood circulation was avoided.     

Molecular basis of severe myoclonic epilepsy in infancy

Severe myoclonic epilepsy (SMEI) or Dravet syndrome is caused by mutations of the SCN1A gene that encodes voltage-gated sodium channel alpha-1 subunit. Recently, we generated and characterized a knock-in (KI) mice with an SCN1A nonsense mutation that appeared in three independent SMEI patients. The SCN1A-KI mice well reproduced the SMEI disease phenotypes. Both homozygous and heterozygous knock-in mice developed epileptic seizures within the first postnatal month. In heterozygous knock-in mice, trains of evoked action potentials in inhibitory neurons exhibited pronounced spike amplitude decrement late in the burst but not in pyramidal neurons. We further showed that in wild-type mice the Nav1.1 protein is expressed dominantly in axons and moderately in somata of parbalbumin (PV) – positive inhibitory interneurons. Our immunohistochemical observations of the Nav1.1 are clearly distinct to the previous studies, and our findings has corrected the view of the Nav1.1 protein distribution. The data indicate that Nav1.1 plays critical roles in the spike output from PV interneurons and further, that the specifically altered function of these inhibitory circuits may contribute to epileptic seizures in the mice. These information should contribute to the understanding of molecular pathomechanism of SMEI and to develop its effective therapies.     

Correlation between scalp-recorded electroencephalographic and electrocorticographic activities during ictal period.

OBJECTIVE: To investigate the correlation between scalp-recorded electroencephalographic (EEG) and electrocorticographic (ECoG) activities during ictal periods. METHODS: Simultaneous EEG and ECoG recordings with chronic subdural electrodes were performed in eight patients with partial epilepsy. RESULTS: In two cases where the ictal ECoG discharges originated in deep brain structures such as the hippocampus and interhemispheric surface of the frontal lobe, ictal discharges could not be detected on EEG until they expanded to the cortex of convexity. In four cases, the ictal onset zones were located in the lateral convexity. When synchronous or near synchronous ictal ECoG discharges with amplitudes of 200-2000muV were recorded on more than 8-15cm(2) of cortex, corresponding discharges were recorded on EEG in these four cases. However, in a case of frontal lobe epilepsy, asynchronous ictal ECoG discharges were recorded on 10 electrodes of convexity but no ictal EEG activity was recorded. Furthermore, in two frontal lobe epilepsy cases, ictal EEG discharges did not always reflect the ictal ECoG spike, but occasionally reflected slow background ECoG activity around the ictal discharges. CONCLUSIONS: Multiple factors such as the width of the cortical area involved, amplitude of ictal discharges and degree of synchronization of electrical potentials play important roles in the appearance of ictal EEG recordings, and the relationship between ictal EEG and ECoG is not straightforward.