Quandoque bonus dormitat Corominas: Sobre arragua, laude, matar

Caro Baroja suggested that Basque arragua ‘melting pot’ goes back etymologically to arrugia ‘gallery in a mine’, a word mentioned by Pliny. This totally aberrant etymology is mentioned by Coromines in both the DCELC and the DCECEH. For laude ‘burial stone’, he follows Covarrubias in accepting laudem ‘praise’, but the more plausible etymology is lapidem ‘stone’. However, when it comes to the etymology of matar ‘to kill’, Coromines rejects Covarrubias’ proposal mactare on behalf of implausible phonetic change; however, mactare was a very popular word, and, despite Coromines’ rejection, has to be considered as the best candidate for an etymology for matar.Keywords: Coromines / Joan, etymology, lexicography, Spanish language, Catalan language, Latin language, Basque language

A new potential oncogenic mutation in the FERM domain of JAK2 in BCR-ABL1 negative and V617F negative chronic myeloproliferative neoplasms (CMPNs) revealed by a comprehensive screening of 17 tyrosine kinase coding genes

BCR/ABL1-negative chronic myeloproliferative neoplasms (CMPNs) are a heterogeneous group of clonal hematological malignancies. Over recent years, some genetic events in tyrosine kinase (TK) genes have been described as causal events of these diseases. To identify new genetic aberrations underlying these diseases, we used denaturing high performance liquid chromatography and fluorescence in situ hybridization (FISH) to analyze 17 genes from two receptor-TK families (III and IV) and from three cytoplasmic-TK families (Syk, Abl, and Jak) on samples from 44 BCR/ABL1-negative and JAK2(V617F)-negative CMPN patients with different clinical phenotypes. Although screening by FISH did not reveal novel chromosomal aberrations, several sequence changes were detected. None of them were frequent events, but we identified a new potential activating mutation in the FERM domain of JAK2(R340Q). None of the germline JAK2(V617F) single-nucleotide polymorphisms detected differed in distribution between patients and control subjects. In summary, data presented here show that these genes are not frequently mutated or rearranged in CMPNs, suggesting that molecular events causing these disorders must be located in other genes