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Human activities have greatly increased the reactive nitrogen in the biosphere, thus profoundly altering global nitrogen cycling. The large increase in nitrogen deposition over the past few decades has led to eutrophication in natural ecosystems, with negative effects on forest health and biodiversity. Recent studies, however, have reported oligotrophication in forest ecosystems, constraining their capacity as carbon sinks. Here we demonstrate the widespread biological transformation of atmospheric reactive nitrogen in the canopies of European forests by combining nitrogen deposition quantification with measurements of the stable isotopes in nitrate and molecular analyses across ten forests through August–October 2016. We estimate that up to 80% of the nitrate reaching the soil via throughfall was derived from canopy nitrification, equivalent to a flux of up to 5.76 kg N ha−1yr−1. We also document the presence of autotrophic nitrifiers on foliar surfaces throughout European forests. Canopy nitrification thus consumes deposited ammonium and increases nitrate inputs to the soil. The results of this study highlight widespread canopy nitrification in European forests and its important contribution to forest nitrogen cycling.

The main goal of the present work is to investigate the modulatory effect of Brassica oleraceaitalica x alboglabra (Bimi®) on gut microbiota composition through an in vitrodigester and an in vivotrial. The digester simulates the entire gastrointestinal digestive process. The maintenance of the microbial population during the stabilization and treatment period was checked by bacteria plate counts The human trial included 15 Spanish adults who included 90 g of Bimi® every two days into their habitual diet. Plate counts showed that the treatment with Bimi® elicits eubiosis, favouring the growth of health promoting gut microbes, as seen on the total anaerobic values In vitroresults showed many short chain fatty acids (SCFAs)-producing bacteria favoured by synergetic effects of the fibres, resistant starch and polyphenols present in Bimi®. The human intervention confirmed some of these results and evidenced an increase in beneficial bacteria such as the genus Lactobacillus, and the species Chistensenella minuta, and Ruminococcus bromii, suggesting that Bimi® is capable of modulating gut microbiota towards a healthier status, with great potential in the management of human disorders related to microbiota dysbiosis.

Gene signatures obtained from microarray experiments may be of use to improve the prediction of brain tumor diagnosis. Nevertheless, automated and objective prediction with accuracy comparable to or better than the gold standard should be convincingly demonstrated for possible clinician uptake of the new methodology. Herewith, we demonstrate that primary brain tumor types can be discriminated using microarray data in an automated and objective way.

The gene pzl-1 from the filamentous fungus Neurospora crassa encodes a putative Ser/Thr protein phosphatase that is reminiscent of the Ppz1/Ppz2 and Pzh1 phosphatases from Saccharomyces cerevisiae and Schizosaccharomyces pombe, respectively. The entire PZL-1 protein, as well as its carboxyl-terminal domain, have been expressed in Escherichia coli as active protein phosphatases. To characterize its cellular role, PZL-1 was also expressed in Sz. pombe and in S. cerevisiae. Expression of PZL-1 in S. cerevisiae from the PPZ1 promoter was able to rescue the altered sensitivity to caffeine and lithium ions of a ppz1 strain. Furthermore, high copy number expression of PZL-1 alleviated the lytic phenotype of a S. cerevisiae slt2/mpk1 mitogen-activated protein (MAP) kinase mutant, similarly to that described for PPZ1, and mimicked the effects of high levels of Ppz1 on cell growth. Expression of PZL-1 in fission yeast from a weak version of the nmt1 promoter fully rescued the growth defect of a pzh1Δ strain in high potassium, but only partially complemented the sodium-hypertolerant phenotype. Strong overexpression of the N. crassa phosphatase in Sz. pombe affected cell growth and morphology. Therefore, PZL-1 appears to fulfil every known function carried out by its S. cerevisiae counterpart, despite the marked divergence in sequence within their NH2-terminal moieties. Copyright © 2000 John Wiley & Sons, Ltd.

The gene pzl‐1from the filamentous fungus Neurospora crassaencodes a putative Ser/Thr protein phosphatase that is reminiscent of the Ppz1/Ppz2 and Pzh1 phosphatases from Saccharomyces cerevisiaeand Schizosaccharomyces pombe, respectively. The entire PZL‐1 protein, as well as its carboxyl‐terminal domain, have been expressed in Escherichia colias active protein phosphatases. To characterize its cellular role, PZL‐1 was also expressed in Sz. pombeand in S. cerevisiae. Expression of PZL‐1 in S. cerevisiaefrom the PPZ1promoter was able to rescue the altered sensitivity to caffeine and lithium ions of a ppz1strain. Furthermore, high copy number expression of PZL‐1 alleviated the lytic phenotype of a S. cerevisiae slt2/mpk1mitogen‐activated protein (MAP) kinase mutant, similarly to that described for PPZ1, and mimicked the effects of high levels of Ppz1 on cell growth. Expression of PZL‐1 in fission yeast from a weak version of the nmt1promoter fully rescued the growth defect of a pzh1Δ strain in high potassium, but only partially complemented the sodium‐hypertolerant phenotype. Strong overexpression of the N. crassaphosphatase in Sz. pombeaffected cell growth and morphology. Therefore, PZL‐1 appears to fulfil every known function carried out by its S. cerevisiaecounterpart, despite the marked divergence in sequence within their NH2‐terminal moieties. Copyright © 2000 John Wiley & Sons, Ltd.

A novel nonsense mutation associated with the skipping of constitutive exon 2 of the 3-hydroxy-3-methylglutaryl-CoA lyase gene was found in two patients, from Portugal and Morocco, with 3-hydroxy-3-methylglutaric acidemia. By reverse transcriptase PCR and single-strand conformational polymorphism a G–T transversion was located, at nucleotide 109, of the 3-hydroxy-3-methylglutaryl-CoA lyase cDNA, within exon 2. Two mRNAs were produced as a result of this nonsense mutation: one of the expected size that contains the premature stop codon UAA, and the other with a deletion of 84 bp corresponding to the whole of exon 2. This deletion produced the loss of the last seven amino acids of the leader peptide and the first 21 amino acids of the mature protein. The nonsense mutation was found in a purine-rich GGAAG sequence, which is equal to, or similar to, others reported to be exonic splicing enhancers (ESE). We suggest that the nonsense mutation may affect a possible ESE on exon 2, which would hinder the splice site selection and facilitate an aberrant splice with the skipping of this exon. Determination by quantitative PCR shows that the ratio of mRNA with the nonsense mutation to the mRNA with the deletion is approx. 3:1.

Hearing loss involves both genetic and environmental factors. A mutation (A1555G) in the mtDNA has been associated with aminoglycoside-induced and nonsyndromic sensorineural deafness. The pathological significance of this mutation in Caucasoid families has not been established, and its relationship with antibiotic treatment is not well understood. We studied 70 Spanish families with sensorineural deafness (36 congenital and 34 late onset) for the mtDNA A1555G mutation. The A1555G mutation was found in 19 families with maternally transmitted deafness but not in the other 51 families or in 200 control subjects. In 12 families all the patients with the A1555G mutation who received aminoglycosides became deaf, representing 30.3% of the deaf patients in these families. None of the deaf patients from seven other families received aminoglycosides. Overall, only 17.7% of the patients with deafness and the A1555G mutation had been treated with aminoglycosides. The age at onset of deafness was lower (median age 5 years, range 1–52 years) in those treated with aminoglycosides than in those who did not receive antibiotics (median age 20 years, range 1–65 years) (P<.001). The mtDNA of these families belongs to haplotypes common in Europeans. These data indicate that the A1555G mutation accounts for a large proportion of the Spanish families with late-onset sensorineural deafness, that the A1555G mutation has an age-dependent penetrance for deafness (enhanced by treatment with aminoglycosides), and that mtDNA backgrounds probably do not play a major role in disease expression.