High biomass yield increases in a primary effluent wastewater phytofiltration are associated to altered leaf morphology and stomatal size in Salix miyabeana

Municipal wastewater treatment using willow ‘phyto’-filtration has the potential for reduced environmental impact compared to conventional treatment practices. However, the physiological adaptations underpinning tolerance to high wastewater irrigation in willow are unknown. A one-hectare phytofiltration plantation established using the Salix miyabeana cultivar ‘SX67’ in Saint-Roch-de-l'Achigan, Quebec, Canada, tested the impact of unirrigated, potable water or two loads of primary effluent wastewater 19 and 30 ML ha−1 yr−1. A nitrogen load of 817 kg N ha−1 from wastewater did not increase soil pore water nitrogen concentrations beyond Quebec drinking water standards. The willow phytofiltration phenotype had increased leaf area (+106–142%) and leaf nitrogen (+94%) which were accompanied by significant increases in chlorophyll a + b content. Wastewater irrigated trees had higher stomatal sizes and a higher stomatal pore index, despite lower stomatal density, resulting in increased stomatal conductance (+42–78%). These developmental responses led to substantial increases in biomass yields of 56–207% and potable water controls revealed the nitrogen load to be necessary for the high productivity of 28–40 t ha−1 yr−1 in wastewater irrigated trees. Collectively, this study suggests phytofiltration plantations could treat primary effluent municipal wastewater at volumes of at least 19 million litres per hectare and benefit from increased yields of sustainable biomass over a two-year coppice cycle. Added-value cultivation practices, such as phytofiltration, have the potential to mitigate negative local and global environmental impact of wastewater treatment while providing valuable services and sustainable bioproducts

Mutations in DCC cause isolated agenesis of the corpus callosum with incomplete penetrance

Brain malformations involving the corpus callosum are common in children with developmental disabilities. We identified DCC mutations in four families and five sporadic individuals with isolated agenesis of the corpus callosum (ACC) without intellectual disability. DCC mutations result in variable dominant phenotypes with decreased penetrance, including mirror movements and ACC associated with a favorable developmental prognosis. Possible phenotypic modifiers include the type and location of mutation and the sex of the individual

Cerebral processing in vegetatieve state II: Auditory stimulation

info:eu-repo/semantics/publishe

Subsidence and strike-slip tectonism of the upper continental slope off Manzanillo, Mexico

The direction of convergence between the Rivera and North American plates becomes progressively more oblique (in a counter-clockwise sense as measured relative to the trench-normal direction) northwestward along the Jalisco subduction zone. By analogy to other subduction zones, the forces resulting from this distribution of convergence directions are expected to produce a NW moving, fore-arc sliver and a NW–SE stretching of the fore-arc area. Also, a series of roughly arc parallel strike-slip faults may form in the fore-arc area, both onshore and offshore, as is observed in the Aleutian arc. In the Jalisco subduction zone, the Jalisco block has been proposed to represent such a fore-arc sliver. However, this proposal has encountered one major problem. Namely, right-lateral strike-slip faulting within the fore-arc sliver, and between the fore-arc sliver and the North American plate, should be observed. However, evidence for the expected right-lateral strike-slip faulting is sparse. Some evidence for right-lateral strike-slip faulting along the Jalisco block–North American plate boundary (the Tepic–Zacoalco rift system) has been reported, although some disagreement exists. Right-lateral strike-slip faulting has also been reported within the interior of the Jalisco block and in the southern Colima rift, which forms the SE boundary of the Jalisco block. Threefold, multi-channel seismic reflection data were collected in the offshore area of the Jalisco subduction zone off Manzanillo in April 2002 during the FAMEX campaign of the N/O L'Atalante. These data provide additional evidence for recent strike-slip motion within the fore-arc region of the Jalisco subduction zone. This faulting offsets right-laterally a prominent horst block within the southern Colima rift, from which we conclude that the sense of motion along the faulting is dextral. These data also provide additional evidence for recent subsidence within the area offshore of Manzanillo, as has been proposed

DCC mutation update: Congenital mirror movements, isolated agenesis of the corpus callosum, and developmental split brain syndrome

The deleted in colorectal cancer (DCC) gene encodes the netrin-1 (NTN1) receptor DCC, a transmembrane protein required for the guidance of commissural axons. Germline DCC mutations disrupt the development of predominantly commissural tracts in the central nervous system (CNS) and cause a spectrum of neurological disorders. Monoallelic, missense, and predicted loss-of-function DCC mutations cause congenital mirror movements, isolated agenesis of the corpus callosum (ACC), or both. Biallelic, predicted loss-of-function DCC mutations cause developmental split brain syndrome (DSBS). Although the underlying molecular mechanisms leading to disease remain poorly understood, they are thought to stem from reduced or perturbed NTN1 signaling. Here, we review the 26 reported DCC mutations associated with abnormal CNS development in humans, including 14 missense and 12 predicted loss-of-function mutations, and discuss their associated clinical characteristics and diagnostic features. We provide an update on the observed genotype-phenotype relationships of congenital mirror movements, isolated ACC and DSBS, and correlate this to our current understanding of the biological function of DCC in the development of the CNS. All mutations and their associated phenotypes were deposited into a locus-specific LOVD (https://databases.lovd.nl/shared/genes/DCC)

Congenital mirror movements: mutational analysis of RAD51 and DCC in 26 cases

Objective: We screened a large series of individuals with congenital mirror movements (CMM) for mutations in the 2 identified causative genes, DCC and RAD51. Methods: We studied 6 familial and 20 simplex CMMcases. Each patient had a standardized neurologic assessment. Analysis of DCC and RAD51 coding regions included Sanger sequencing and a quantitative method allowing detection of micro rearrangements. We then compared the frequency of rare variants predicted to be pathogenic by either the PolyPhen-2 or the SIFT algorithm in our population and in the 4,300 controls of European origin on the Exome Variant Server. Results: We found 3 novel truncating mutations of DCC that segregate with CMM in 4 of the 6 families. Among the 20 simplex cases, we found one exonic deletion of DCC, one DCC mutation leading to a frameshift, = missense variants in DCC, and 2 missense variants in RAD51. All 7 missense variants were predicted to be pathogenic by one or both algorithms. Statistical analysis showed that the frequency of variants predicted to be deleterious was significantly different between patients and controls (p < 0.001 for both RAD51 and DCC). Conclusion: Mutations and variants in DCC and RAD51 are strongly associated with CMM, but additional genes causing CMM remain to be discovered. © 2014 American Academy of Neurology

Mutations in the netrin-1 gene cause congenital mirror movements

Netrin-1 is a secreted protein that was first identified 20 years ago as an axon guidance molecule that regulates midline crossing in the CNS. It plays critical roles in various tissues throughout development and is implicated in tumorigenesis and inflammation in adulthood. Despite extensive studies, no inherited human disease has been directly associated with mutations in NTN1, the gene coding for netrin-1. Here, we have identified 3 mutations in exon 7 of NTN1 in 2 unrelated families and 1 sporadic case with isolated congenital mirror movements (CMM), a disorder characterized by involuntary movements of one hand that mirror intentional movements of the opposite hand. Given the diverse roles of netrin-1, the absence of manifestations other than CMM in NTN1 mutation carriers was unexpected. Using multimodal approaches, we discovered that the anatomy of the corticospinal tract (CST) is abnormal in patients with NTN1-mutant CMM. When expressed in HEK293 or stable HeLa cells, the 3 mutated netrin-1 proteins were almost exclusively detected in the intracellular compartment, contrary to WT netrin-1, which is detected in both intracellular and extracellular compartments. Since netrin-1 is a diffusible extracellular cue, the pathophysiology likely involves its loss of function and subsequent disruption of axon guidance, resulting in abnormal decussation of the CST