Composts as alternative to inorganic fertilization for cereal crops.

The use of treated organic products as fertilizers and soil amendments not only results in economic benefits for the small-scale farmer, but it also reduces pollution due to reduced nutrient run-off and N leaching. In this work, the feasibility of using composts as fertilizers and soil improvers has been evaluated at the field level, in barley and soft wheat crops (two successive cultivations of each crop). The applied treatments consisted of two commercial composts (compost manure and sewage sludge compost) added to the soil either alone (T1 and T3) or in combination with inorganic fertilizers (T2 and T4) and a conventional mineral fertilization (T5). Physical, physical-chemical, chemical, microbiological, and biochemical parameters were determined in the soil after each harvest. In both barley and wheat crops, soils treated with composts showed higher organic C, humic substances, and humic acid contents than the inorganically fertilized soil, as well as higher contents of water-soluble P, K, Ca, Mg, and S. In both successive crops, all treatments led to similar yields of total barley and wheat vegetal material (straw + ears) and grain, differences between treatments being not statistically significant (p ≤ 0.05). Organically treated soils showed higher microbial size and activity than inorganically treated soils as well as higher water-holding capacity. It can be concluded that quality organic composts can be used, at suitable rates, alone or in combination with inorganic fertilizers, as a good alternative to inorganic fertilization for cereal cultivation, improving soil characteristics while giving similar yield and crop quality than conventional inorganic fertilization.

Genetic changes including gene copy number alterations and their relation to prognosis in childhood acute myeloid leukemia.

We studied a series of 68 subjects diagnosed with childhood acute myeloid leukemia (AML) using conventional cytogenetics and fluorescence in situ hybridization (FISH), polymerase chain reaction (PCR) to analyze mutations in FLT3 and NPM1 genes, and/or array comparative genomic hybridization (CGH). Cytogenetic/FISH abnormalities were observed in 71% of subjects, FLT3-ITD mutations in 15%, and NPM1 mutations in 13%. The array CGH alterations (average 3.6 per case) were observed in 96% of the tested subjects. The most frequent alterations were gains of 8q24.3 and 11p15.5-p15.4 in 16% of the samples. Six genes (AKT1, RUNX1, LTB, SDC1, RUNX1T1, and JAK2) from the imbalanced regions have been reported to be involved in AML, whereas other 30 cancer genes, not previously reported in an AML context, were identified as imbalanced. They probably correspond to non passenger alterations that cooperate with the recurrent translocations. The clinical data and genetic changes were tested to find out the possible association with prognosis. Genomic instability (four or more genomic imbalances) was correlated with poor patient outcome (p = 0.029).

[Prader Willi syndrome patients: study of 77 patients]. / Síndrome de Prader Willi: estudio de 77 pacientes.

BACKGROUND: The Prader-Willi syndrome (PWS) is a disease of genetic origin. It is characterized by neonatal hypotonia, hypogonadism, hiperfagia leading to obesity, low stature, developmental delay, moderate mental retardation, abnormal behavior and characteristic facial appearance. It is caused by the loss or the inactivation of paternal genes of the imprinted region 15q11-13. There are different genetic causes: paternal 15q11-q13 deletion in 70% of patients, maternal uniparental disomy in the 20-25% and less than 5% have an imprinting defect. We present the results obtained in the transverse clinical - genetic study of 77 PWS patients. PATIENTS AND METHODS: There has been realized the study of 374 suspected PWS patients. Cytogenetics studies of bands G and hybridization in situ fluorescent (FISH) and molecular genetics analysis of microsatellites, Southern blot, MS-PCR and sequenciation were carried out. Holm's criteria use for the correlation phenotype - genotype in 48 patients. RESULTS: PWS was confirmed in 77 patients, 46 deletion, 16 uniparental disomy, two imprinting defect and 13 only PWS methylation pattern. Significant differences do not observe in the correlation phenotype - genotype. CONCLUSIONS: The frequencies of the molecular alterations, 71.87 % deletion, 25 % UPD and 3.12 % DI, they are similar to described in the literature. It presents the algorithm of diagnosis used with the MS-PCR as rapid technology to confirm PWS.