The safety and efficacy of endoluminal stenting in treating atherosclerotic vertebral artery disease was evaluated in 38 vessels in 32 patients. Indications for revascularization included diplopia (n = 4), blurred vision (n = 4), dizziness (n = 23), transient ischemic attacks (n = 4), drop attack (n = 1), gait disturbance (n = 1), headache (n = 2), and asymptomatic critical stenosis (n = 1). Success (< 20% residual diameter stenosis, without stroke or death) was achieved in all 32 patients (100%). One patient experienced a transient ischemic attack (TIA) 1 hr after the procedure. At follow-up (mean, 10.6 months), all patients (100%) were alive and 31/32 (97%) were asymptomatic. One patient (3%) had in-stent restenosis at 3.5 months and underwent successful balloon angioplasty. Endoluminal stenting of vertebral artery lesions is safe, effective, and durable as evidenced by the low recurrence rate. Primary stent placement is an attractive option for atherosclerotic vertebral artery stenotic lesions. Cathet Cardiovasc Intervent 2001;54:1-5.

SUMMARY1. The Vaseline-gap technique was used to record calcium currents (ICa) and charge movement in single cut fibres from normal human muscle. Experiments were carried out in 2 or 10 mM-extracellular Ca2" concentration ([Ca2+].) and at 17 or 27 'C.2. The passive electrical properties of the fibres with this technique were: membrane resistance for unit length rm = 59-4 kQ cm; longitudinal resistance per unit length ri = 4-9 MQ/cm; longitudinal resistance per unit length under the Vaseline seals re = 438 MC/cm; specific membrane resistance Rm = 1-176 kQ cm2; input capacitance = 5-53 nF; specific membrane capacitance = 8-9 ,uF/cm2 . and k = 15-2 mV. 9. The fact that the activation curves of the ICa and the charge movement differ widely in the mid-point of activation can be explained by the presence of several closed states before the channel opens. In addition, it is also possible that only part of the charge movement corresponds to the gating of the Ca2+ channel.

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Objective. To investigate the metabolism of L-tryptophan (LT) via the kynurenine pathway in patients with the eosinophilia-myalgia syndrome (EMS).Methods. Measurement of LT, L-kynurenine, and quinolinic acid in plasma and cerebrospinal fluid (CSF) from subjects with EMS, from asymptomatic users of LT, and from normal subjects.Results. Plasma LT concentrations were lower in untreated EMS patients (n = 5 ) than in corticosteroidtreated EMS patients (n = 5; P < 0.05) and in asymptomatic users of LT (n = 5; P < 0.05). Untreated EMS patients, who had discontinued LT weeks to months prior to study, had significantly higher plasma levels of L-kynurenine and quinolinic acid than did corticosteroid-treated EMS patients (P < 0.05), normal subjects (P C 0.02), and asymptomatic users of LT (P < 0.05). ~~From EMS patients also had significantly elevated levels of L-kynurenine (P < 0.05) and quinolinic acid (P < 0.001) in CSF compared with normal subjects. After a l-gm oral dose of LT, untreated EMS patients (n = 4)showed lower peak levels of LT and accentuated synthesis of L-kynurenine and quinolinic acid, compared with these values in corticosteroid-treated EMS patients (n = 2), who responded like normal subjects (n = 5).Conclusion. These data demonstrate that during the active phase of EMS, LT metabolism via the kynurenine pathway was accentuated, probably secondary to induction of the enzyme indoleamine-2,3-dioxygenase. Ingestion of large amounts of LT (median daily dose 1.5 gm) resulted in high concentrations of kynureninepathway metabolites in blood and extrahepatic tissues, which was accentuated in EMS patients and which may have played a significant role in the pathogenesis of the disease.The eosinophilia-myalgia syndrome (EMS) is a recently described illness that reached epidemic proportions in the United States in the late summer and fall of 1989 ( I ) , and was subsequently shown to be associated with the ingestion of contaminated lots of L-tryptophan (LT) (2,3). Although one contaminant has been characterized ( I , 1 '-ethylidenebis[ L-tryptophan]) (41, it has not been determined whether this is the etiologic agent or merely a marker for an as-yetunidentified agent. The mechanism by which this contamination induces EMS is unknown.Several factors suggest that L-tryptophan or one of its metabolites may be important in the pathogenesis of EMS. First, the contaminant epidemiologically linked to EMS is an LT analog. Second, abnormal metabolism of LT has been identified in several