Recent studies have proposed that n-3 polyunsaturated fatty acids (n-3 PUFAs) have direct antioxidant and anti-inflammatory effects in vascular tissue, explaining their cardioprotective effects. However, the molecular mechanisms are not yet fully understood. We tested whether n-3 PUFAs showed antioxidant activity through the activation of nuclear factor erythroid 2-related factor 2 (Nrf2), a master transcriptional factor for antioxidant genes. C57BL/6 or Nrf2−/− mice were fed a fish-oil diet for 3 weeks. Fish-oil diet significantly increased the expression of heme oxygenase-1 (HO-1), and endothelium-dependent vasodilation in the aorta of C57BL/6 mice, but not in the Nrf2−/− mice. Furthermore, we observed that 4-hydroxy hexenal (4-HHE), an end-product of n-3 PUFA peroxidation, was significantly increased in the aorta of C57BL/6 mice, accompanied by intra-aortic predominant increase in docosahexaenoic acid (DHA) rather than that in eicosapentaenoic acid (EPA). Human umbilical vein endothelial cells were incubated with DHA or EPA. We found that DHA, but not EPA, markedly increased intracellular 4-HHE, and nuclear expression and DNA binding of Nrf2. Both DHA and 4-HHE also increased the expressions of Nrf2 target genes including HO-1, and the siRNA of Nrf2 abolished these effects. Furthermore, DHA prevented oxidant-induced cellular damage or reactive oxygen species production, and these effects were disappeared by an HO-1 inhibitor or the siRNA of Nrf2. Thus, we found protective effects of DHA through Nrf2 activation in vascular tissue, accompanied by intra-vascular increases in 4-HHE, which may explain the mechanism of the cardioprotective effects of DHA.

We report three cases showing body lateropulsion as the sole or predominant symptom of caudal lateral medullary infarction. All of them presented a small infarction on the lateral surface of the caudal medulla corresponding to the dorsal spinocerebellar tract (DSCT). IntroductionLateropulsion is known to be one of the symptoms of lateral medullary infarctions (LMIs). Although it is usually associated with ipsilateral Horner syndrome, ipsilateral limb ataxia, superficial sensory disturbance of the ipsilateral face and contralateral limbs, dysarthria, dysphagia, and vertigo, isolated body lateropulsion is rare. Although the lesion responsible for lateropulsion is controversial (1), recent studies (2-4) have identified possible corresponding lesions for lateropulsion. Here, we present three cases of caudal LMIs in which lateropulsion was the sole or predominant manifestation. Although lateropulsion due to LMIs is reported to improve within a few weeks (4), the condition of one of our patients progressed to typical Wallenberg syndrome. Case Report Case 1A 78-year-old woman noted acute lateropulsion to the right on June 16, 2002. She had diabetes mellitus and angina pectoris. On examination, there was no vertigo, nystagmus, hearing deficit, dysarthria, dysphagia, deficit in either superficial or deep sensation, ophthalmoplegia, Horner syndrome, hemiparesis, or limb ataxia. Magnetic resonance imaging (MRI) showed a fresh small infarction selectively involving the right superficial lateral portion of the caudal medulla (Fig. 1A). MR angiography showed stenosis of the right vertebral artery. Her symptom slowly resolved within two weeks. Case 2A 76-year-old man experienced lateropulsion to the right on January 9, 2003. He was receiving medication for hypertension. He showed no vertigo, nystagmus, hearing loss, dysarthria, dysphagia, sensory loss, ophthalmoplegia, Horner syndrome, or hemiparesis. MRI showed a fresh small infarction situated in the same position as in Case 1 (Fig. 1B). MR angiography showed weak flow in the vertebral arteries. Three days later, vomiting, decreased temperature sensation on the right face and the left limbs and trunk, and right Horner syndrome appeared abruptly. MRI revealed expansion of the infarct area (Fig. 1C). The lateropulsion itself improved within two weeks. Case 3An 84-year-old man presented with acute onset of veering of his body to the right on February 20, 2004. He was receiving medication for hypertension and diabetes mellitus. He did not have vertigo, nausea, or tinnitus, nor did he have hoarseness, dysphagia, or dysarthria. There was no ophthalmoplegia, Horner syndrome, limb ataxia, or hemiparesis. Pain and thermal sensations were decreased on his right face and over the contralateral side of his body. MRI showed a

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