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El uso continuado de los fungicidas tiabendazol e imazalil en los empaques citrícolas de la región del río Uruguay ha llevado a la selección y proliferación de aislamientos de moho verde resistentes; este hongo es la principal causa de podredumbres en poscosecha. Recientemente, el fungicida pirimetanil (anilino-pirimidina) (PYR) se ha incorporado a los programas de control de esta enfermedad. El objetivo del presente trabajo fue estudiar la resistencia a este fungicida de una colección de aislamientos, obtenida luego de que este principio activo se incorporara a los programas de control en los empaques citrícolas durante un período de aproximadamente 5 años. 122 aislamientos de moho verde fueron recolectados desde Monte Caseros (Corrientes) hasta Concordia (Entre Ríos) durante 2015. Estos fueron obtenidos de frutos con síntomas del patógeno en campo y empaque. Se determinó la concentración de PYR que reduce el crecimiento de las colonias en un 50% (EC50) para cada aislamiento. La EC50 media de los aislamientos recolectados en campo fue de 0,16 ± 0,02 μg mL-1. No se observaron aislamientos resistentes en campo donde el fungicida no es usado. Por el contrario, el 64,4% de los aislamientos recolectados en empaques se muestran resistentes a PYR, con una EC50 media de 5,51 ± 0,37 μg mL-1. Los sensibles presentan una EC50 media de 0,20 ± 0,02 μg mL-1. La información suministrada en este trabajo resulta importante en el monitoreo de la susceptibilidad del moho verde al fungicida PYR en la región citrícola del río Uruguay. La incorporación de este fungicida en los programas de control de moho verde debe hacerse en forma cuidadosa, implementando distintas estrategias para lograr resultados efectivos. The continuous use of the fungicides thiabendazol and imazalil in the citrus packing houses of the Uruguay River region has led to the selection and proliferation of resistant green mold isolates, being this fungus the main cause of postharvest rot. Recently, the fungicide pyrimethanil (anilino-pyrimidine) (PYR) has been incorporated into the control programs of this disease. The objective of the present work was to study the resistance to this fungicide of a collection of isolates, obtained after this active principle was incorporated into control programs in the citrus packaging houses during a period of approximately 5 years. 122 green mold isolates were collected from Monte Caseros (Corrientes) to Concordia (Entre Ríos) during 2015. They were obtained from fruits with symptoms of the pathogen in the field and packaging. The concentration of PYR which reduces colony growth by 50% (EC50) was determined for each isolation. The mean EC50 of the field-collected isolates was 0.16 ± 0.02 μg mL-1. No resistant isolates were observed in the field where the fungicide is not used. In contrast, 64.4% of those collected from packing houses were resistant to PYR, with an average EC50 5.51 ± 0.37 μg mL-1. Those sensible isolates showed an EC50 mean 0.20 ± 0.02 μg mL-1. The information provided in this work is important for monitoring susceptibility of green mold to the fungicide PYR in the citrus region of the Uruguay River. The incorporation of this fungicide in green mold control programs must be done carefully, and different strategies must be implemented to achieve effective results. EEA Concordia Fil: Panozzo, Marina Graciela. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Concordia; Argentina Fil: Almiron, Nanci Jacqueline. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Concordia; Argentina Fil: Bello, Fernando. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Concordia; Argentina Fil: Vazquez, Daniel Eduardo. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Concordia; Argentina

Objective: To evaluate the family history of epilepsy in first degree relatives of probands with epilepsy. Methods: A sample of 10787 patients with epilepsy with complete information about first degree relatives (parents, siblings and offspring) was selected from the database of the Episcreen Project, the largest Italian observational study on epilepsy. Family history was assessed by: (1) prevalence estimates of epilepsy among proband's relatives, (2) modified cumulative risks (MCR), adjusted using proband's age as censoring time in life tables, (3) standardised morbidity ratios (SMR), using a sub-group of symptomatic epilepsies as control group. Results: Patients (9.1%) had a family history of epilepsy. The overall prevalence of epilepsy among first degree relatives was 2.6%. Idiopathic generalised epilepsies had the highest prevalence (5.3%). Cryptogenetic epilepsies had a lower prevalence (2.1%) than idiopathic epilepsies, but higher then symptomatic epilepsies (1.5%), both in generalised and focal forms (3.8% vs. 2.0% and 1.8% vs. 1.3%). A similar tendency was detected using MCR and SMR, with the higher values of risks/ratios for idiopathic and generalised epilepsies. Probands with idiopathic generalised epilepsies were highly concordant with respect to their relatives' type of epilepsy. Considering other strata factors, risks were higher in proband's epilepsies with an onset less then 14 years of age, while sex played no definite role in differentiating the family history. Conclusions: The Episcreen model permits a variety of stratification factors to measure family risk, including age at onset, epilepsy localisation and aetiology with a large sample of more than 10000 probands and 1065/40544 relatives affected and classified.

A reduced glucose tolerance or frank diabetes mellitus is a frequent finding in patients with pancreatic cancer. The aim of this study was to verify whether the pancreatic cancer cell line MIA PaCa2 was able to produce any factor which could induce hyperglycemia in SCID (severe complete immunodeficient) mice. MIA PaCa2 cells were cultured in Dulbecco's modified Eagle's medium (DMEM) for 7 days. Twenty-five female SCID mice were used. They were daily i.p. injected with 300 ul of cell culture supernatants (Group T, n = 13) or with 300 ul of DMEM (Group C, n = 12) and followed up for 82 days. Blood glucose levels were significantly higher in Group T than in Group C on days 10 and 25. Intravenous glucose tolerance test, success-fully performed in 9 animals (4 controls and 5 treated), demonstrated a significantly reduced glucose tolerance in Group T compared to Group C mice. At sacrifice, plasma and pancreatic insulin and glucagon levels did not vary between groups. The ratio between pancreatic and plasma insulin was significantly lower in Group T than in Group C. We conclude that: 1. The pancreatic cancer cell line MIA PaCa2 produces one or more soluble factors able to cause hyperglycemia in vivo; 2. this effect is not immunologically mediated, and 3. this/these factor/s could both interfere with the pancreatic beta cells and/or with insulin peripheral action.

Lipid peroxidation is one of the most important expression of oxidative stress induced by oxygen-derived free radicals. Here we evaluate the behavior of malondialdehyde (MDA) in the serum and urine from patients with chronic pancreatic diseases, with respect to patients with extra-pancreatic digestive diseases and glomerulonephritis. Serum and urinary phospholipase A2 (PLA2) activity was also determined, since this enzyme contributes to damage of plasma membranes. MDA and PLA2 levels increased in the sera from most of the patients with pancreatic and extra-pancreatic digestive diseases. In glomerulonephritis, pathological MDA levels (36%), but not PLA2 levels, were found. Serum MDA correlated with gamma-glutamyl transpeptidase (GGT), while PLA2 correlated with alanine-phosphodiesterase (ALP), GGT, alanine-aminotransferase (ALT) and creatinine. In urine, MDA and PLA2 behaved differently from the corresponding serum values. MDA increased in some patients with pancreatic cancer, extra-pancreatic diseases and glomerulonephritis. PLA2 levels did not significantly vary between groups. Urinary MDA correlated with some indicators of renal tubular damage [urinary ribonuclease, beta-2-microglobulin (B-2-M) and N-acetyl-glucosaminidase (NGA)] and with serum bilirubin. Urinary PLA2 correlated only with ribonuclease (RNase). We conclude that serum MDA increases aspecifically in pancreatic and extra-pancreatic diseases, probably reflecting an aspecific phlogistic phenomenon; PLA2, although sharing a similar pattern with MDA, seems mainly related to hepato-biliary damage. Urinary MDA reflects the presence of renal tubular damage, which may be the cause or a consequence of lipid peroxidation; little variations in PLA2 are recorded in urine, and mainly reflect the presence of impaired tubular function.

The pathogenetic mechanism underlying glucose intolerance in pancreatic cancer is still unclear. We studied the pattern of three glucose regulating hormones (C-peptide, glucagon and GH) in pancreatic cancer patients with (N = 34) and without (N = 8) hyperglycemia, and compared the findings made with those from subjects with other hyperglycemic conditions of well-known origin [type I diabetes mellitus (8 cases) and diabetes mellitus secondary to chronic pancreatitis (13 cases) or liver cirrhosis (4 cases)]. In hyperglycemic pancreatic cancer patients, C-peptide was absent in 26% of the cases, reduced in 24%, elevated in 29% and within the normal range in the remaining 21%. In normoglycemic pancreatic cancer this hormone was reduced in two cases (25%) and within the normal range in all the others. GH was within the normal range in all cases: glucagon was below the normal range in some hyperglycemic pancreatic cancer patients (41%) or within the normal range in all the remaining patients. No correlations were found between the three hormones when findings from subjects were considered all together. However, in pancreatic cancer C-peptide and glucagon presented consensual variations. C-peptide, glucagon and GH levels were not related to tumor volume; glucagon was found to be associated with liver metastases. C-peptide was correlated with serum ALT and ALP. We may conclude that hyperglycemia associated with pancreatic cancer may be caused by different mechanisms. In some cases a reduced secretion of both insulin and glucagon was observed, as occurs in chronic pancreatitis. In the majority of patients, beta cell function appears normal, and the hyperglycemic state may depend on an altered peripheral sensitivity to insulin due to the pancreatic pathology itself or to consensual liver involvement.

Renal cell carcinoma is a neoplasia with an unpredictable behavior. Nuclear grade and pathologic stage are widely accepted as valuable prognostic factors. More recently DNA content has been proposed as an adjunctive parameter of the clinical course of the disease. In order to substantiate these findings we prospectively analyzed 36 frozen specimens from patients submitted to radical nephrectomy for renal cell carcinoma. The study population had a 2:1 male/female ratio with a median age of 57 years. Six of 33 patients died of tumor progression with a median survival time of 11 months. The tumor DNA index (DI) ranged from 0.86 to 2.06 with a mean coefficient of variation of 4.59. Ten cases (27.8%) had a diploid DNA content, whereas 26 (72.2%) showed a distinct aneuploid population. In 10 cases different DI values were observed in different samples from the same tumor. Aneuploidy was significantly associated with advanced pathologic stages, high nuclear grade, and tumor progression.