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Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a heterogeneous disease in which diverse autoantibodies have been described but systematic screening has never been performed. Detection of CIDP-specific antibodies may be clinically useful. We developed a screening protocol to uncover novel reactivities in CIDP. Sixty-five CIDP patients and 28 controls were included in our study. Three patients (4.6%) had antibodies against neurofascin 155, four (6.2%) against contactin-1 and one (1.5%) against the contactin-1/contactin-associated protein-1 complex. Eleven (18.6%) patients showed anti-ganglioside antibodies, and one (1.6%) antibodies against peripheral myelin protein 2. No antibodies against myelin protein zero, contactin-2/contactin-associated protein-2 complex, neuronal cell adhesion molecule, gliomedin or the voltage-gated sodium channel were detected. In IgG experiments, three patients (5.3%) showed a weak reactivity against motor neurons; 14 (24.6%) reacted against DRG neurons, four of them strongly (7.0%), and seven (12.3%) reacted against Schwann cells, three of them strongly (5.3%). In IgM experiments, six patients (10.7%) reacted against DRG neurons, while three (5.4%) reacted against Schwann cells. However, results were not statistically significant when compared to controls. Immunoprecipitation experiments identified CD9 and L1CAM as potential antigens, but reactivity could not be confirmed with cell-based assays. In summary, we describe a diverse autoantibody repertoire in CIDP patients, reinforcing the hypothesis of CIDP's pathophysiological heterogeneity.Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a disabling disease with a pathogenesis that remains largely unknown 1 . CIDP response to immune therapies and scarce experimental evidence on passive transfer animal models suggest that humoral factors play a role in its pathogenesis 2 . CIDP diagnosis is based on clinical and electrophysiological criteria 3 that allow the inclusion of a broad spectrum of patients within CIDP, including typical and atypical variants. This heterogeneity has hindered the description of disease-specific biomarkers, despite intensive research efforts 4 .The response of CIDP patients to intravenous immunoglobulin (IVIg) and plasma exchange (PlEx) suggests that humoral factors are involved in its pathogenesis. The search of autoantibodies has been the most important laboratory research topic in CIDP. Initial focus was placed on myelin antigens. Classical studies, using diverse techniques, detected higher frequencies of antibodies against myelin protein zero (MPZ), peripheral myelin protein 2 (PMP2) or peripheral myelin protein 22 (PMP22) [5][6][7][8][9][10] . However, meaningful clinical-immunological correlations with those antigens were not established. CIDP patients harboring antibodies against LM1-containing

There is an increasing interest in the involvement of trace elements such as zinc in the pathogenesis of cardiovascular diseases. This study was designed to examine whether moderate zinc deficiency during growth influences blood pressure (BP) and vascular nitric oxide (NO) pathway. Three-week-old weaned male Wistar rats were randomly divided into two dietary groups and fed either a moderately zinc-deficient diet (zinc content 9 mg/kg; n ϭ 12) or a control diet (zinc content 30 mg/kg; n ϭ 12) for 60 d. The following were measured: systolic BP, nitrates and nitrites urinary excretion, urinary chemiluminescence intensity, NADPH-diaphorase activity in the thoracic aorta and intestinal arterioles, and NO synthase (NOS) catalytic activity using L-[U14C]-arginine as substrate in the thoracic aorta. Zinc deficiency during growth induced an increase in BP from day 30 of the experimental period, leading to hypertension on day 60. Animals that were fed the zinc-deficient diet had lower urinary excretion levels of nitrates and nitrites and higher intensity of spontaneous luminescence on day 60. At the end of the experiment, zinc-deficient rats showed decreased NADPH diaphorase activity in endothelium and smooth muscle of the thoracic aorta and intestinal arterioles and decreased activity of NOS in thoracic aortic tissue. An imbalance in zinc bioavailability during postnatal and growing periods may be may be a risk factor in development of cardiovascular alterations in adult life. The mechanisms involved may include an impaired vascular NO system as a result of decreased NOS activity and higher systemic oxidative stress. Moderate and marginal zinc deficiency is by far more common than severe deficiency, especially in infants, children, and pregnant women in developing and developed countries, as a result of imbalances between intake and increased requirements (1,2). Zinc is an essential trace element required by all living organisms for many physiologic functions, including growth, development, and reproduction (3). Zinc has been documented to act as an antioxidant, to have membranestabilizing properties, to block apoptotic cell death, and to be essential for endothelial integrity (4 -6). Intracellular zinc is associated with proteins, primarily via complex interactions with cysteines, acting as an integral component of numerous metalloenzymes, structural proteins, and transcription factors (1,7).There is increasing interest in possible involvement of trace elements such as zinc in the pathogenesis of cardiovascular diseases (8). Many enzymes that are involved in the regulation of arterial blood pressure (BP), such as nitric oxide (NO) synthase (NOS), angiotensin-converting enzyme, and neutral endopeptidases, contain zinc in their structure (9 -11). The NOSs are a family of enzymes that catalyze the synthesis of NO and L-citrulline from L-arginine in the presence of NADPH and O 2 . The NOS family consists of three isoforms that are expressed in many tissues, including endothelium and vascular

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SUMMARYObjectives: To validate and translate the English version of the Neurologic Depression Disorders Inventory in Epilepsy (NDDI-E) into Spanish as a screening instrument for major depressive episodes (MDE) for patients with epilepsy from Argentina and Uruguay. Methods: One hundred fifty-five consecutive outpatients with epilepsy participated in this study. The module of MDE of the MINI International Neuropsychiatric Instrument (MINI Plus version) was used as the gold standard against which the translated version of the NDDI-E was validated. Results: Among the 155 patients, 25 (16%) met Diagnostic and Statistical Manual, Fourth Edition (DSM-IV) criteria for MDE according to the MINI. With a total score of >15, The NDDI-E identified MDE with an 80% sensitivity, 90% specificity, 60% positive predictive value, and 95.5% negative predictive value. Significance: These data indicate that the Spanish version of the NDDI-E can reliably identify MDE in patients with epilepsy from Argentina and Uruguay.