Produção e desenvolvimento de colônias de abelhas africanizadas (Apis mellifera l.) a partir de diferentes áreas e idades de cria Production and development of africanized honey bee (Apis mellifera l.) colonies departing from different comb brood areas and brood ages

A apicultura brasileira usa da captura de enxames silvestres de abelhas melíferas africanizadas (Apis mellifera L.) para repor e/ou aumentar o número de colônias dos apiários, possuindo inconvenientes como a dependência da natureza para captura dos enxames, a heterogeneidade genética das colônias capturadas e a possibilidade desses enxames serem portadores de doenças e parasitas prejudiciais à sanidade das abelhas. O presente trabalho testa e apresenta uma técnica de divisão de colônias de abelhas melíferas africanizadas para a produção de novas colônias fortes em curto espaço de tempo, a partir de recursos mínimos de cera, cria e alimento. Os resultados mostraram que núcleos de A. mellifera formados inicialmente com uma rainha jovem e fecundada, 1 kg de operárias, um quadro de cria fechada, um quadro de favo puxado e vazio e dois quadros com cera alveolada permitem a produção de novas colônias em 42 dias. Portanto, pode-se concluir que a técnica de divisão de colônias por formação de núcleos como descrito acima, oferece aos apicultores uma alternativa viável para a produção e comercialização em larga escala de novas colônias de abelhas melíferas africanizadas.<br>The Brazilian apiculture relies upon collecting wild swarms of Africanized honey bees (Apis mellifera L.) to replace and/or increase the number of colonies in the apiaries. This practice brings problems such as dependence on nature to capture any swarm, diverse genetic make-up of the colonies captured and the possibility of these swarms be carrying diseases and parasites harmful to the bees. The present work tests and presents a technique to split colonies of Africanized honey bees to produce new strong colonies in short time, departing from little resources of wax, brood and food stores. Results showed that A. mellifera nuclei formed by a young and mated queen, 1kg of workers, a frame of sealed brood, an empty frame of drawn beeswax and two frames containing an embossed sheet of beeswax each, allows producing new colonies within 42 days. Therefore, it is concluded that the technique to split colonies in nuclei as described above gives beekeepers a viable alternative to produce and commercialize new colonies of Africanized honey bees in large scale

A search for doubly charged higgs production in z0 decays

Contains fulltext : 124394.pdf (preprint version ) (Open Access

Rare mutations in SQSTM1 modify susceptibility to frontotemporal lobar degeneration

Mutations in the gene coding for Sequestosome 1 (SQSTM1) have been genetically associated with amyotrophic lateral sclerosis (ALS) and Paget disease of bone. In the present study, we analyzed the SQSTM1 coding sequence for mutations in an extended cohort of 1,808 patients with frontotemporal lobar degeneration (FTLD), ascertained within the European Early-Onset Dementia consortium. As control dataset, we sequenced 1,625 European control individuals and analyzed whole-exome sequence data of 2,274 German individuals (total n = 3,899). Association of rare SQSTM1 mutations was calculated in a meta-analysis of 4,332 FTLD and 10,240 control alleles. We identified 25 coding variants in FTLD patients of which 10 have not been described. Fifteen mutations were absent in the control individuals (carrier frequency <0.00026) whilst the others were rare in both patients and control individuals. When pooling all variants with a minor allele frequency <0.01, an overall frequency of 3.2 % was calculated in patients. Rare variant association analysis between patients and controls showed no difference over the whole protein, but suggested that rare mutations clustering in the UBA domain of SQSTM1 may influence disease susceptibility by doubling the risk for FTLD (RR = 2.18 [95 % CI 1.24-3.85]; corrected p value = 0.042). Detailed histopathology demonstrated that mutations in SQSTM1 associate with widespread neuronal and glial phospho-TDP-43 pathology. With this study, we provide further evidence for a putative role of rare mutations in SQSTM1 in the genetic etiology of FTLD and showed that, comparable to other FTLD/ALS genes, SQSTM1 mutations are associated with TDP-43 pathology