Zeolitized tuffs in pedotechnique for the reclamation of abandoned quarries. A case study in the Campania region (Italy).

The present study aims to assess the evolution of different proto-horizons as embryonic soils built by pedotechnologies for the reclamation and management of derelict and damaged lands, such as abandoned quarries. The model proto-horizons were assembled by utilizing coarse limestone gravel or zeolitized Phlegraean Yellow Tuff (PYT) as mineral components and commercial compost-amendments or a phosphorite-poultry manure mixture as organic matrices for growth of a pasture-grass under controlled conditions. The evolution of the model proto-horizons was followed by an evaluation of the stability and modification of the organic matter (OM) with reference to plant development. The results suggest that the natural carbonatic substrate occurring in limestone quarries was unable to sustain significant plant growth, while the PYT was suitable and efficient as a pedogenic substrate because it supported plant growth and induced a conspicuous accumulation of OM due to root activity. In particular, OM, including humic and non-humic components, greatly increased in the PYT treatment with the phosphorite-poultry manure mixture showing a concurrent trend toward humification. Conversely, an overall tendency toward degradation of OM was detected in the PYT model proto-horizon treated with commercial compost. Feasibility estimates show that quarry restoration costs appear reasonable where environmental impacts are high.

Lack of serotonin1B receptor expression leads to age-related motor dysfunction, early onset of brain molecular aging and reduced longevity.

Normal aging of the brain differs from pathological conditions and is associated with increased risk for psychiatric and neurological disorders. In addition to its role in the etiology and treatment of mood disorders, altered serotonin (5-HT) signaling is considered a contributing factor to aging; however, no causative role has been identified in aging. We hypothesized that a deregulation of the 5-HT system would reveal its contribution to age-related processes and investigated behavioral and molecular changes throughout adult life in mice lacking the regulatory presynaptic 5-HT(1B) receptor (5-HT(1B)R), a candidate gene for 5-HT-mediated age-related functions. We show that the lack of 5-HT(1B)R (Htr1b(KO) mice) induced an early age-related motor decline and resulted in decreased longevity. Analysis of life-long transcriptome changes revealed an early and global shift of the gene expression signature of aging in the brain of Htr1b(KO) mice. Moreover, molecular changes reached an apparent maximum effect at 18-months in Htr1b(KO) mice, corresponding to the onset of early death in that group. A comparative analysis with our previous characterization of aging in the human brain revealed a phylogenetic conservation of age-effect from mice to humans, and confirmed the early onset of molecular aging in Htr1b(KO) mice. Potential mechanisms appear independent of known central mechanisms (Bdnf, inflammation), but may include interactions with previously identified age-related systems (IGF-1, sirtuins). In summary, our findings suggest that the onset of age-related events can be influenced by altered 5-HT function, thus identifying 5-HT as a modulator of brain aging, and suggesting age-related consequences to chronic manipulation of 5-HT.

Specificity and timing of neocortical transcriptome changes in response to BDNF gene ablation during embryogenesis or adulthood.

Brain-derived neurotrophic factor (BDNF) has been reported to be critical for the development of cortical inhibitory neurons. However, the effect of BDNF on the expression of transcripts whose protein products are involved in gamma amino butric acid (GABA) neurotransmission has not been assessed. In this study, gene expression profiling using oligonucleotide microarrays was performed in prefrontal cortical tissue from mice with inducible deletions of BDNF. Both embryonic and adulthood ablation of BDNF gave rise to many shared transcriptome changes. BDNF appeared to be required to maintain gene expression in the SST-NPY-TAC1 subclass of GABA neurons, although the absence of BDNF did not alter their general phenotype as inhibitory neurons. Furthermore, we observed expression alterations in genes encoding early-immediate genes (ARC, EGR1, EGR2, FOS, DUSP1, DUSP6) and critical cellular signaling systems (CDKN1c, CCND2, CAMK1g, RGS4). These BDNF-dependent gene expression changes may illuminate the biological basis for transcriptome changes observed in certain human brain disorders.