Effects of the current financial and economic crisis on the rural landscape as well as the agri-food sector in Europe and Central Asia

This paper reviews the expected effects of the current financial crisis and subsequent recession on the rural landscape, in particular the agri-food sector in Europe and Central Asia (ECA) on the basis of the structure of the rural economy and of different organisations and institutions. Empirical evidence suggests that the crisis has hit the ECA region the hardest. Agriculture contributes about 9% to gross domestic product (GDP) for the ECA region as a whole with 16% of the population being employed in the agricultural sector. As far as the impact of the financial crisis on the agri-food sector is concerned, there are a few interconnected issues: (1) reduction in income elastic food demand and commodity price decline, (2) loss of employment and earnings of rural people working in urban centres, implying also costly labour reallocation, (3) rising rural poverty originating mainly from lack of opportunities in the non-farm sector and a sizable decline of international remittances, (4) tightening of agricultural credit markets, and the (5) collapse of sectoral government support programs and social safety-net measures in many countries. The paper reveals how the crisis hit farming and broader agri-business differently in general and in the ECA sub-regions

First magmatism in the New England Batholith, Australia: forearc and arc–back-arc components in the Bakers Creek Suite gabbros

The New England Orogen, eastern Australia, was established as an outboard extension of the Lachlan Orogen through the migration of magmatism into forearc basin and accretionary prism sediments. Widespread S-type granitic rocks of the Hillgrove and Bundarra supersuites represent the first pulse of magmatism, followed by I- and A-types typical of circum-Pacific extensional accretionary orogens. Associated with the former are a number of small tholeiite–gabbroic to intermediate bodies of the Bakers Creek Suite, which sample the heat source for production of granitic magmas and are potential tectonic markers indicating why magmatism moved into the forearc and accretionary complexes rather than rifting the old Lachlan Orogen arc. The Bakers Creek Suite gabbros capture an early ( ∼  305 Ma) forearc basalt-like component with low Th ∕ Nb and with high Y ∕ Zr and Ba ∕ La, recording melting in the mantle wedge with little involvement of a slab flux and indicating forearc rifting. Subsequently, arc–back-arc like gabbroic magmas (305–304 Ma) were emplaced, followed by compositionally diverse magmatism leading up to the main S-type granitic intrusion ( ∼  290 Ma). This trend in magmatic evolution implicates forearc and other mantle wedge melts in the heating and melting of fertile accretion complex sediments and relatively long ( ∼  10 Myr) timescales for such melting

Steam Reforming Technology for Denitration and Immobilization of DOE Tank Wastes

THOR Treatment Technologies, LLC (THOR) is a joint venture formed in June 2002 by Studsvik, Inc. (Studsvik) and Westinghouse Government Environmental Services Company LLC to further develop, market, and deploy Studsvik's patented THORSM non-incineration, steam reforming waste treatment technology. This paper provides an overview of the THORSM steam reforming process as applied to the denitration and conversion of Department of Energy (DOE) tank wastes to an immobilized mineral form. Using the THORSM steam reforming technology to treat nitrate containing tank wastes could significantly benefit the DOE by reducing capital and life-cycle costs, reducing processing and programmatic risks, and positioning the DOE to meet or exceed its stakeholder commitments for tank closure. Specifically, use of the THORSM technology can facilitate processing of up to 75% of tank wastes without the use of vitrification, yielding substantial life-cycle cost savings

Histomorphometric evaluation of bone healing in rabbit fibular osteotomy model without fixation

<p>Abstract</p> <p>Background</p> <p>Animal models of fracture consolidation are fundamental for the understanding of the biological process of bone repair in humans, but histological studies are rare and provide only qualitative results. The objective of this article is to present the histomorphometric study of the bone healing process using an experimental model of osteotomy in rabbit fibula without interference of synthesis material.</p> <p>Methods</p> <p>Fifteen rabbits were submitted to fibular osteotomy without any fixation device. Groups of five animals were submitted to pharmacological euthanasia during a period of one (group A), two (group B) and four weeks (group C) after osteotomy. Histomorphometric evaluation was performed in the histological sections.</p> <p>Results</p> <p>During week one there was intense cellularity (67/field), a large amount of woven bone (75.7%) and a small amount of lamellar bone (7.65%). At two weeks there was a decrease in woven bone (41.59%) and an increase in lamellar bone (15.16%). At four weeks there was a decrease of cellularity (19.17/field) and lamellar bone (55.56%) exceeded the quantity of woven bone (31.68%).</p> <p>Conclusion</p> <p>Histomorphometric (quantitative) evaluation of the present study was shown to be compatible with bone healing achieved in qualitative experimental models that have been commended in the literature.</p

Revisiting the university front

dc.subject: Postdemocracy / Public function of the university / Governance / Knowledge society / research university / Managerialism / Academic audit / Quality contro

Novel C8orf37 mutations cause retinitis pigmentosa in consanguineous families of Pakistani origin

Purpose: To investigate the molecular basis of retinitis pigmentosa in two consanguineous families of Pakistani origin with multiple affected members. Methods: Homozygosity mapping and Sanger sequencing of candidate genes were performed in one family while the other was analyzed with whole exome next-generation sequencing. A minigene splicing assay was used to confirm the splicing defects. Results: In family MA48, a novel homozygous nucleotide substitution in C8orf37, c.244–2A>C, that disrupted the consensus splice acceptor site of exon 3 was found. The minigene splicing assay revealed that this mutation activated a cryptic splice site within exon 3, causing a 22 bp deletion in the transcript that is predicted to lead to a frameshift followed by premature protein truncation. In family MA13, a novel homozygous null mutation in C8orf37, c.555G>A, p.W185*, was identified. Both mutations segregated with the disease phenotype as expected in a recessive manner and were absent in 8,244 unrelated individuals of South Asian origin. Conclusions: In this report, we describe C8orf37 mutations that cause retinal dystrophy in two families of Pakistani origin, contributing further data on the phenotype and the spectrum of mutations in this form of retinitis pigmentosa

Targeted nanopore sequencing enables complete characterisation of structural deletions initially identified using exon-based short-read sequencing strategies

Background The widespread adoption of exome sequencing has greatly increased the rate of genetic diagnosis for inherited conditions. However, the detection and validation of large deletions remains challenging. While numerous bioinformatics approaches have been developed to detect deletions from whole - exome sequencing and targeted panels, further work is typically required to define the physical breakpoints or integration sites. Accurate characterisation requires either expensive follow - up whole - genome sequencing or the time - consuming, laborious process of PCR walking, both of which are challenging when dealing with the repeat sequences which frequently intersect deletion breakpoints. The aim of this study was to develop a cost-effective, long-range sequencing method to characterise deletions. Methods Genomic DNA was amplified with primers spanning the deletion using long-range PCR and the products purified. Sequencing was performed on MinION flongle flowcells. The resulting fast5 files were basecalled using Guppy, trimmed using Porechop and aligned using Minimap2. Filtering was performed using NanoFilt. Nanopore sequencing results were verified by Sanger sequencing. Results Four cases with deletions detected following comparative read-depth analysis of targeted short-read sequencing were analysed. Nanopore sequencing defined breakpoints at the molecular level in all cases including homozygous breakpoints in EYS, CNGA1 and CNGB1 and a heterozygous deletion in PRPF31. All breakpoints were verified by Sanger sequencing. Conclusions In this study, a quick, accurate and cost - effective method is described to characterise deletions identified from exome, and similar data, using nanopore sequencing

Specific Alleles of CLN7/MFSD8, a Protein That Localizes to Photoreceptor Synaptic Terminals, Cause a Spectrum of Nonsyndromic Retinal Dystrophy

Purpose: Recessive mutations in CLN7/MFSD8 usually cause variant late-infantile onset neuronal ceroid lipofuscinosis (vLINCL), a poorly understood neurodegenerative condition, though mutations may also cause nonsyndromic maculopathy. A series of 12 patients with nonsyndromic retinopathy due to novel CLN7/MFSD8 mutation combinations were investigated in this study. Methods: Affected patients and their family members were recruited in ophthalmic clinics at each center where they were examined by retinal imaging and detailed electrophysiology. Whole exome or genome next generation sequencing was performed on genomic DNA from at least one affected family member. Immunofluorescence confocal microscopy of murine retina cross-sections were used to localize the protein. Results: Compound heterozygous alleles were identified in six cases, one of which was always p.Glu336Gln. Such combinations resulted in isolated macular disease. Six further cases were homozygous for the variant p.Met454Thr, identified as a founder mutation of South Asian origin. Those patients had widespread generalized retinal disease, characterized by electroretinography as a rod-cone dystrophy with severe macular involvement. In addition, the photopic single flash electroretinograms demonstrated a reduced b- to a-wave amplitude ratio, suggesting dysfunction occurring after phototransduction. Immunohistology identified MFSD8 in the outer plexiform layer of the retina, a site rich in photoreceptor synapses. Conclusions: This study highlights a hierarchy of MFSD8 variant severity, predicting three consequences of mutation: (1) nonsyndromic localized maculopathy, (2) nonsyndromic widespread retinopathy, or (3) syndromic neurological disease. The data also shed light on the underlying pathogenesis by implicating the photoreceptor synaptic terminals as the major site of retinal disease