Laparoscopic transhiatal approach for resection of midesophageal diverticula.

Resection of symptomatic midesophageal diverticula is traditionally performed with a thoracic approach, occasionally requiring additional laparoscopic surgery for management of associated pathologies, such as esophageal dysmotility and hiatus hernia. We present the resection of large midesophageal pulsion diverticula using a single laparoscopic transhiatal approach. Bariatric instrumentation was used to obtain extra intraoperative length, and concurrent on-table endoscopy was performed to ensure complete mucosal seal. The patient was discharged home on day 19 and remains well 12 months after surgery. Laparoscopic transhiatal resection of symptomatic midesophageal diverticula may be a safe alternative to the traditional thoracic or thoracoabdominal technique.

A missense mutation in kynurenine aminotransferase-1 in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) are the most extensively used animal model for genetic hypertension, increased stroke damage, and insulin resistance syndromes; however, the identification of target genes has proved difficult. SHR show elevated sympathetic nerve activity, and stimulation of the central blood pressure control centers with glutamate or nicotine results in exaggerated blood pressure responses, effects that appear to be genetically determined. Kynurenic acid, a competitive glutamate antagonist and a non-competitive nicotinic antagonist, can be synthesized in the brain by the enzyme kynurenine aminotransferase-1 (KAT-1). We have previously shown that KAT-1 activity is significantly reduced in SHR compared with normotensive Wistar Kyoto rats (WKY). Here we show that KAT-1 contains a missense mutation, E61G, in all the strains of SHR examined but not in any of the WKY or outbred strains. Previous studies on F2 rats from a cross of stroke-prone SHR and WKY have shown a suggestive level of linkage between elevated blood pressure and the KAT-1 locus on chromosome 3. In addition, the mutant enzyme expressed in Escherichia coli displays altered kinetics. This mutation may explain the enhanced sensitivity to glutamate and nicotine seen in SHR that may be related to an underlying mechanism of hypertension and increased sensitivity to stroke.